Found 160 Abstracts
CONTROL ID: 1700175
TITLE: SlimQuick™- Associated Hepatotoxicity Resulting in Fulminant Liver Failure
PRESENTER: Dina Halegoua-De Marzio
PRESENTER (INSTITUTION ONLY): Thomas Jefferson University Hospital
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: There have been many reports of toxicity associated with use of dietary supplements; some of these cases
have lead to fatal outcomes. We report a rare case of fulminant liver failure assumed to be from ingestion of
SlimQuick™ (Wellnx Life Sciences, Wilmington, DE) weight loss supplement containing green tea extract (GTE).
Case Report: A 52-year-old woman presented to the Emergency Department with one week of vomiting and
progressive jaundice. On further questioning, the patient reported two days of ingesting the weight loss supplement
SlimQuick™ while fasting 3 weeks before presentation. Past medical, surgical and family histories were
unremarkable. Physical examination showed normal mental status, icteric sclera, mild abdominal distension and lower
extremity edema. Initial workup showed total bilirubin of 16.5 mg/dL, AST 1507 IU/L, ALT 945 IU/L, alkaline
phosphatase 210 IU/L and INR 2.82. CT abdomen revealed nodular liver with small amount of ascites. Serological
tests for viral hepatitis, autoimmune hepatitis, Wilson disease, and primary biliary cirrhosis were negative. Liver biopsy
was consistent with confluent hepatic necrosis with collapse. In the unlikely possibility that there was an autoimmune
etiology to her acute liver injury, Prednisone 60mg was initiated but discontinued two days later due to worsening liver
function. A day later, the patient’s mental status began to deteriorate. The patient was expeditiously evaluated and
listed for liver transplant. She underwent liver transplantation two days later. The patient was discharged home postoperative day eight.
Discussion: To our knowledge, this is the first reported case of fulminant liver due to ingestion of SlimQuick™. The
major ingredient in SlimQuick™ is GTE. GTE is a common ingredient in several dietary supplements, some of which
have been withdrawn from the market due to safety concerns. An example of this is Exolise® (Arkopharma, France), a
weight loss supplement containing GTE that was withdrawn from the market due to 13 cases of liver injury. Since
1966, 34 case reports of liver toxicity with GTE were identified by the United States Pharmacopeia. The majority of
cases present with an acute hepatocellular injury pattern and most recover with cessation of use. An idiosyncratic or
an immune-allergic mechanism appears to be the likely mechanism of injury. Animal studies with high doses of GTE
have described dose dependent hepatotoxicity resulting in severe morbidity and mortality. This demonstrates the
importance obtaining herbal and dietary supplement history in previously healthy subjects who develop liver injury.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: Yes
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Dina Halegoua-De Marzio : ACG Member
Simona Rossi : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1700196
TITLE: Reversible, Complete Unilateral Sensorineural Hearing Loss During Treatment with Telaprevir, Pegylated
Interferon and Ribavirin for Chronic Hepatitis C
PRESENTER: Joseph Yarze
PRESENTER (INSTITUTION ONLY): Gastroenterology Associates of Northern New York
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: CASE REPORT: An otherwise healthy 57-year-old male had a history of hepatitis C, which was initially
diagnosed in 1994. It was presumably contracted through IVDU, between approximately 1970 and 1984. A liver
biopsy in November, 2003 revealed A0/F0 disease, and a decision for expectant management was made. Chronic
hepatitis C was of high–titer and type IB genotype. A repeat liver biopsy in February 2012 revealed A3/F3 disease,
and at that juncture, it was recommended that he undergo a trial of hepatitis C antiviral therapy.
Treatment began with telaprevir (750 mg po Q8 hrs), pegylated interferon (PEG-IFN) alpha-2a (180 micrograms sq Q
wk), ribavirin (600 mg po BID). Treatment initially ensued uneventfully, and after 4 weeks of therapy, the patient was a
complete rapid virologic responder with undetectable HCV RNA. After 8 weeks of therapy, there was mild rash,
presumably related to telaprevir. This was treated with topical corticosteroid (0.05% fluocinonide) cream, with gradual
improvement. After 12 weeks of therapy, hepatitis C RNA remained undetectable. Given advanced fibrosis, a 48-week
course of treatment was anticipated. The patient subsequently developed mild pancytopenia, which did not require
dosage reduction of antiviral therapy.
After 26 weeks of treatment, the patient developed acute unilateral hearing loss. At this juncture, PEG-IFN and
ribavirin were promptly discontinued (telaprevir had been discontinued per protocol after 12 weeks of therapy) and
ENT consultation was sought. Audiometric testing revealed moderate to severe, middle and high frequency
sensorineural hearing loss in the left ear. A 2-week course of corticosteroid therapy was empirically prescribed
(prednisone 50 mg po QD, tapered over 14 d). There was rapid improvement and full recovery of hearing over 2
weeks. A repeat audiometric test performed three weeks later revealed normalization. No further antiviral therapy was
prescribed. Despite the attenuated course of therapy for hepatitis C, the patient was ultimately proven to be a
sustained virologic responder.
CONCLUSION: Acute sensorineural hearing loss may be associated with hepatitis C antiviral therapy. Other case
reports would suggest that this rare clinical scenario is most likely IFN–related. As has been noted in most other
reported cases, the hearing loss was unilateral, and auditory recovery occurred after discontinuation of antiviral
therapy. It remains unclear whether the empiric course of corticosteroid therapy was in part responsible for the
favorable clinical outcome.
Methods: n/a
Results: n/a
Conclusion: n/a
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Joseph Yarze : ACG Member
Michael DeVito : ACG Non-Member
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AVERAGE SCORE: 4.5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1701201
TITLE: A Malignant Case Of Gastrointestinal Bleeding
PRESENTER: Dipendra Chaudhary
PRESENTER (INSTITUTION ONLY): Wake Forest University Health Sciences
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 32-year-old female was referred for management of severe anemia due to gastrointestinal bleeding, and
hemoptysis with lung and liver lesions. She underwent EGD, which revealed active bleeding in the stomach,
duodenum, and jejunum secondary to diffuse mucosal vascular lesions, which were treated with cauterization.
Capsule endoscopy and push enteroscopy revealed similar findings. PET CT scan was negative. Bone marrow biopsy
revealed hypercellular marrow without evidence of malignancy. A suspected diagnosis of hereditary hemorrhagic
telengectesias (HHT) was made, and was started on estrogen-progesterone, aminocaproic acid, and Avastin
(bevacizumab). Despite transfusion, the patient had progressive gastrointestinal bleeding. She developed fulminant
DIC and was transfused factors, platelets, but subsequently developed multiorgan system failure. Given the poor
prognosis, the family decided to withdraw life-sustaining measures, and she expired shortly afterwards. Autopsy was
consistent with metastatic angiosarcoma to the gastrointestinal tract, lungs, and spleen, with probable liver primary.
Immunohistochemistry was positive for CD31 and CD34, and negative for human herpes virus 8 (HHV 8), making
Kaposi’s sarcoma unlikely. Gene sequence of ACVRL1, ENG, and SMAD4 specific for HHT was negative in
antemortem blood samples. Vascular lesions evaluated were not consistent with AVMs.
Discussion: Hepatic angiosarcomas are rare, and constitute about 2% of all sarcomas. Predisposing factors for
angiosarcomas include chronic exposure to thorium dioxide, vinyl chloride, and arsenic. Angiosarcoma is known to
have protean distribution affecting multiple organ systems, including skin, soft tissue, heart, great vessels, breast, or
liver. Bleeding is the most common presentation of this disease, given the vascular nature of the lesion.
Histopathologically, these tumours are highly vascular, with abundance of endothelial cells and areas of solid and
spindled cell tumour with an infiltrative and destructive growth pattern. These tumours express endothelial markers,
including CD34 and CD31. Surgical resection is the primary mode of treatment. Doxorubicin and taxol-based
chemotherapies have shown promising results; however, early diagnosis and surgical resection remains the best
approach.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Dipendra Chaudhary : ACG Non-Member
IMAGE CAPTION:
(no table selected)
AVERAGE SCORE: 3.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: Unique case!|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego: [No
Comments]
CONTROL ID: 1701223
TITLE: Methimazole-Related Hepatotoxicity
PRESENTER: Joseph Yarze
PRESENTER (INSTITUTION ONLY): Gastroenterology Associates of Northern New York
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Case Report: A 45-year-old female with recently diagnosed hyperthyroidism presented with abnormal liver
biochemical tests. She was healthy and on no medications until she presented with an eight-week history of a 20-lb
unintentional weight loss, periorbital edema, feeling anxious, tremor and hair loss. Hyperthyroidism was rapidly
diagnosed on a clinical basis with supportive bloodwork results, and a metabolic profile initially showed normal liver
biochemical tests. Atenolol (25 mg po QD) was prescribed and further testing ensued over the next four weeks, which
included thyroid scanning and sonography. Grave’s disease was firmly diagnosed and repeat liver biochemical testing
was again normal. Methimazole (20 mg po QD) was then prescribed. The patient was noted to have abnormal LFTs 1
week after starting methimazole, with a serum total bilirubin 1.7 (N=0.2-1.0 mg/dl), alkaline phosphatase 252 (N=50136 U/L), AST 130 (N=12-32 U/L) and ALT 511 (N=20-65 U/L). The CBC revealed normal values. The patient noted
itching and darkening of her urine over the next week, and methimazole was discontinued (while atenolol was
continued). Two weeks after discontinuing methimazole, the total bilirubin peaked at 3.8, alkaline phosphatase 325,
AST 279 and ALT 769. The PT INR was normal on multiple occasions. RUQ sonography revealed a normal liver, no
gallstones and lack of biliary dilation. Serologic/virologic testing for acute hepatitis A, B, C and E were negative.
Markers for autoimmune hepatitis and PBC were negative. Methimazole-induced cholestatic hepatitis was
presumptively diagnosed. Given the clinical scenario, liver biopsy was not pursued. Pruritis worsened and an
antihistamine (cyproheptadine four mg po TID) and ursodeoxycholic acid (600 mg po BID) were prescribed. Over the
ensuing six weeks, mild jaundice resolved and the liver biochemical tests completely normalized. Resolution of pruritis
lagged behind improvement of the LFT’s, but completely resolved a few weeks later. Given concerns for future
potential hepatotoxicity related to propylthiouracil, the patient was then treated with radioiodine therapy, and she did
well clinically.
Conclusion: Methimazole has been reported to infrequently cause idiosyncratic hepatotoxicity. The pattern is usually
one of cholestatic hepatitis, and uneventful recovery after drug withdrawal is generally noted.
Methods: n/a
Results: n/a
Conclusion: n/a
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Joseph Yarze : ACG Member
Jennifer Beller : ACG Non-Member
(No Image Selected)
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AVERAGE SCORE: 5.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1712471
TITLE: An Unusual Case of Cirrhosis
PRESENTER: Ahmad Alkaddour
PRESENTER (INSTITUTION ONLY): University of Florida
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 49-year-old white female with history of sarcoidosis was referred to GI when her liver was noted to be
nodular during laparoscopy for an ovarian cyst. She denied fatigue, hematemesis, abdominal distension and pain,
ankle swelling, itching, yellow discoloration of skin and eyes and episodes of confusion or sleepiness. She denied
alcohol abuse. Physical examination revealed normal VS and no icterus, spider nevi, clubbing, ascites,
hepatosplenomegaly or edema. LFTs revealed mild elevation in alkaline phosphatase and PT was slightly prolonged.
CBC showed mild thrombocytopenia. Hepatitis serologies, ANA, AMA, ASMA, Ferritin, Ceruloplasmin, and α1-AT
level were unremarkable. A liver biopsy confirmed cirrhosis. Biopsy did not show any granulomas, but showed
sinusoidal dilatation, which prompted a referral to cardiology. ECHO showed enlarged IVC and was otherwise
unremarkable. A left and right heart catheterization was done. LHC showed normal coronaries, and RHC showed RAP
12 mm Hg, PAP 32/15 (mean 21) mm Hg, PAWP 18 mm Hg, LVEDP 18 mm Hg and CO 5.2 l/min. She developed
worsening shortness of breath and was referred to pulmonology here. PFTs showed mild restriction, but CXR was
unrevealing. CTPA ruled out PE and showed scattered pericardial calcification. Bubble ECHO did not show a right to
left shunt. She developed SVT and was hospitalized here. She underwent a repeat left and right heart catheterization:
RAP was 25 mm Hg, PAP 52/25 (mean 37) mm Hg, PAWP 32 mm Hg, LVEDP 36 mm Hg, and CO 4.12 l/min.
Simultaneous measurement of left and right sided pressures confirmed constrictive pericarditis. In retrospect, the
cirrhosis is “cardiac” cirrhosis and the result of long-standing elevated right sided heart pressures. Similarly, her
dyspnea on exertion can be explained by constrictive pericarditis. We believe that constrictive pericarditis resulted
from Sarcoidosis. She is now being evaluated for pericardiectomy.
Clinical Pearls:
1.A cardiac etiology should be considered in the work up of cirrhosis especially when the most common causes are
not found.
2.Pericardial calcification should suggest the possibility of constrictive pericarditis.
3.Simultaneous measurement of left and right sided pressures should be performed when there is suspicion of
constrictive pericarditis.
4.Sarcoidosis is a rare but well known cause of pericardial disease.
Methods: n/a
Results: n/a
Conclusion: n/a
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Ahmad Alkaddour : ACG Non-Member
Adil Shujaat : ACG Non-Member
IMAGE CAPTION:
(no table selected)
AVERAGE SCORE: 3.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1718008
TITLE: Portal Hypertension and Ascites Secondary to Erdheim Chester Disease without Intrinsic Liver Involvement on
Liver Biopsy
PRESENTER: Donald Tsynman
PRESENTER (INSTITUTION ONLY): University of Rochester
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Case: A 49-year-old male with dyspnea, fatigue and bloating was found to have a pericardial effusion in the
ED. Pericardiocentesis was inconclusive for etiology. One month later, dyspnea recurred and a CT chest and
abdomen showed a new left pleural effusion. VATs with biopsies revealed non-specific inflammatory cells. As an
outpatient, he had worsening renal function and continued to note vague abdominal pain. Subsequent CT revealed
new ascites, hepatosplenomegaly and a soft tissue mantle surrounding the aorta and bilateral iliac arteries. Labs
revealed Albumin 3.4, ALT 66, AST 42, Alk Phos 570, T. Bili 0.3 and GGT 86. A perinephric biopsy revealed a
fibrohistiocytic proliferation histologically compatible with Erdheim Chester Disease (ECD). PET scan was suggestive
of liver involvement. The patient subsequently began interferon. After four weeks of tx, the patient was requiring
weekly LVPs. Indirect portal pressure gradient measurements suggested simultaneous moderate post-hepatic and
sinusoidal portal hypertension. The biopsy revealed a periportal inflammatory infiltrate and fibrosis with vascular tissue
(including hepatic vein) demonstrating chronic inflammatory cells CD68 positive and negative for S100 and CD1a
staining consistent with ECD. Mild steatohepatitis and a neutrophilic ductitis were present, but there was no inherent
cirrhosis or histiocytosis of the liver parenchyma. Consequently, it was thought that his portal hypertension was related
to the effects of the EC-associated histiocyte infiltrate on the hepatic vasculature, which led to increased post-hepatic
and sinusoidal pressures without parenchymal disease.
Discussion: First described by Austrian pathologist Jakob Erdheim and American pathologist William Chester in 1930,
ECD is a process of xanthogranulomatous infiltration of tissues with foamy histiocytes in the absence of langerhans
cells. This leads to a concomitant fibrosis. Approximately 250 cases have ever been reported. Liver involvement has
seldom been described. Even fewer cases have reported ascites as a part of the syndrome. None have tried to
delineate the etiology of the ascites. Specifically interesting in our case is that the sequelae of portal hypertension, as
aforementioned in our patient, possibly occurred not as a result of direct damage to the hepatic parenchyma, but
rather due to infiltration of the hepatic vasculature by the disease. In addition to treatment focused on the patient’s
underlying histiocytosis with interferon, a plan to supplement albumin and improve nutritional status eventually helped
to decrease the patient’s need for therapeutic paracenteses. This, consequently, allowed for safe discharge home
where he has continued interferon treatment.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Donald Tsynman : ACG Member
Curtis Weaver : ACG Member
Erik Olson : ACG Non-Member
Sofia Taboada : ACG Non-Member
Jennifer Findeis-Hosey : ACG Non-Member
Benedict Maliakkal : ACG Member
Jonathan Huang : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3.5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1719524
TITLE: Hepatogastric Fistula following Transcatheter Arterial Embolization of HCC: A Case Report
PRESENTER: Miles Dunbar
PRESENTER (INSTITUTION ONLY): University of MS Medical center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction: Hepatogastric fistula(HGF) is a rare but serious complication of Transcatheter arterial
embolization [TAE ] of hepatic artery for Hepatocellular Carcinoma. We present a case of 51-year-old male with HCC,
who developed HGF following TAE and later succumbed to the complications from HCC.
Case report: A 51-year-old male with chronic hepatitis B, cirrhosis and biopsy-proven hepatocellular carcinoma who
initially presented with right upper quadrant pain, epigastric mass and approximately 20 lb weight loss over a short
period of time. CT abdomen showed a heterogeneous hypervascular mass arising in the lateral segment of the left
lower lobe of the liver. He subsequently underwent TAE of the hepatic mass, which later was complicated by liver
abcess that was subsequently drained by Interventional Radiology. The patient presented again for his second
chemoembolization, during which he complained of melena and coffee ground emesis. Gastroenterology(GI) was
consulted, and upper Endoscopy [EGD] revealed a 2-cm ulcer on the lesser curvature of stomach, which
communicated with the liver and was believed to be hepatocellular cancer mass. Surgery was consulted and
recommended supportive care, as the disease was far advanced. GI recommendations included proton pump
inhibitors and avoidance of any NG tubes. The patient was discharged to the hospice care.
Discussion: HGF is a rare but serious complication after TAE and radiotherapy for HCC. Development of fever,
abdominal pain and jaundice after an initial symptom-free interval following TAE should elicit the suspicion of
Hepatogastric fistula formation from a necrotic HCC or a ruptured liver abscess. Patients with risk factors, including
liver cirrhosis and large lesions close to the adjacent gastrointestinal tract, are especially vulnerable.
TAE has become the mainstay among non-surgical treatment modalities for the management of unresectable HCC.
Due to incomplete tumor necrosis following single TAE, it is often necessary to perform TAE several times at regular
intervals.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Inderpreet Grover : ACG Non-Member
Miles Dunbar : ACG Non-Member
Naveed Ahmad : ACG Non-Member
HGF
IMAGE CAPTION: HGF
(no table selected)
AVERAGE SCORE: 4.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1722508
TITLE: Herpes Simplex Virus (HSV) Hepatitis and Acute Liver Failure In A Seemingly Immunocompetent Patient
PRESENTER: Matt Kaspar
PRESENTER (INSTITUTION ONLY): VCU
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction: Development of systemic HSV infection, including hepatitis, is typically seen in
immunocompromised patients (HIV, malignancy, immunosuppressive treatment, malnutrition, pregnancy, advanced
age). HSV hepatitis is characteristically an anicteric hepatitis with markedly elevated aminotransferases (> 3000) and
frequent systemic symptoms (fever). High index of clinical suspicion is very important, since HSV hepatitis can be
associated with high mortality, and prompt treatment with Acyclovir can be life-saving. Recognizing HSV hepatitis is
particularly important in patients without known risk factors for HSV dissemination. Diagnosing HSV hepatitis in such
patients should prompt a search for the presence of an indolent immune compromise.
Case: We present a case of a 55-year-old Caucasian male with no significant medical history who presented with
eight days of fever, rigors, nausea, and vomiting. Physical exam: BP 97/61, HR 80, T 101.6, macular rash on the face
and chest; otherwise unremarkable. He was started on broad spectrum antibiotics for presumed infection, but his fever
continued. On hospital day two, he developed confusion and somnolence; ammonia was 37. Mental status improved
with lactulose. The patient developed vesicular rash on the back during the hospital stay.
Initial lab work-up revealed WBC 6, aminotransferases 700s, bilirubin 1.4, INR 1.1. Blood and urine cultures, hepatitis
A/B/C serology, ANA, AMA, immunoglobulins, HIV, EBV, and CMV were all negative. Acute HSV serology, however,
was positive, and HSV-1 DNA was positive as well. Aminotransferases continued to increase: by hospital day six,
AST and ALT had risen to 3,800 and 1,700; INR to 1.5; bilirubin remained 1.4. Atypical lymphocytes and smudge cells
were repeatedly noted on peripheral smear.
Abdominal CT scan showed mild ascites and pancreatic, portal, and caval lymphadenopathy. Liver biopsy was
performed, and revealed well-circumscribed foci of coagulative necrosis consistent with herpes viral injury;
immunohistochemical stain was strongly positive for HSV within the necrotic areas. A swab from a vesicle on the
back tested positive for HSV by direct flourescent antibody test.
Therapy with IV Acyclovir was initiated, with rapid improvement in clinical status, aminotransferases, and
coagulopathy.
The persistent evidence of atypical lymphocytes and smudge cells in this patient with HSV hepatitis justified additional
workup. The patient was found to have monoclonal gammopathy and chronic lymphocytic leukemia, for which he is
currently being followed up by Hematology.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Matt Kaspar : ACG Non-Member
M. Thure Caire : ACG Non-Member
Sanjay Bangarulingam : ACG Non-Member
Iliana Bouneva : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1722564
TITLE: Benign Hyperbilirubinemia: A Rare Liver Involvement in Sickle Cell Disease
PRESENTER: Luis Quiel
PRESENTER (INSTITUTION ONLY): Metropolitan Hospital Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: There are three well-documented liver involvements in sickle cell disease. The uncommon variant, known as
benign hyperbilirubinemia, has only nine cases described in the literature [1] and, were managed conservatively. We
describe a case of benign hyperbilirubinemia managed with exchange transfusion without any complications; the
bilirubin normalized within two months.
A 20-year-old African-American male with history of sickle cell disease came to the emergency room complaining of
severe right upper quadrant pain, nausea and vomiting. Vital signs were unremarkable; physical examination showed
scleral jaundice and enlarge liver two cm below the costal border that was tender to palpation. The rest of the exam
was unremarkable. Laboratory exams revealed alanine aminotransferase and aspartate aminotransferase were 400
and 333mg/dl respectively, total bilirubin was 20.69mg/dl, direct bilirubin was 6.77mg/dl and alkaline phosphatase of
145mg/dl. Markers of hemolysis were positive. An ultrasound showed hepatomegaly.
Two days from admission, he developed protracted vomiting. MRCP showed normal common bile duct with tiny
gallstones and sludge. Transaminases where trending down, HbS was 91%. The total bilirubin was 20.55 mg/dl with
increased direct levels of 12mg/dl. The lactate dehydrogenase and haptoglobin were normalizing. INR and
hemoglobin were stable during hospital course. Screening for viral hepatitis and autoimmune etiologies were negative.
The patient was managed with anti-emetics and intravenous fluids.
On the third day of hospitalization, the patient was asymptomatic. However, the direct bilirubin level trended up to
21.93 mg/dl.
Exchange transfusion with 16 Units of packed red blood cells was performed. HBS was 19.2%. The direct bilirubin
returned to normal values after two months. No hemolysis was appreciated during follow up.
Liver disease is prevalent in sickle cell disease. It has been estimated that hepatic complications affect 10 to 40% of
hospital admissions due to sickle cell disease [2]. Benign hyperbilirubinemia was described as an increase of bilirubin
with moderate increase in transaminases and alkaline phosphatase levels, and no impairment of plasma coagulation
panel [1]. Those cases where managed without exchange transfusion and the bilirubin levels persisted elevated for a
period of two months [3].
We describe a case of benign hyperbilirubinemia managed with total exchange transfusion, and our result suggests
that there is no change on the outcome, compared with the other cases described in the literature.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Luis Quiel : ACG Non-Member
Gonzalo Olivares : ACG Non-Member
Alexander Sy : ACG Non-Member
Susan Williams : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1726330
TITLE: Hepatocellular Type of Liver Injury After the Use of Azithromycin: A Variant Form of Liver Damage
PRESENTER: Alberto Revelo
PRESENTER (INSTITUTION ONLY): New York Medical College- Metropolitan Hospital Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction: The annual incidence of drug induced liver injury (DILI) is estimated to be 1-10/100,000
persons exposed. A cholestatic pattern of injury has been described with the use of azithromycin. We now present a
case of hepatocellular damage after its use.
Case: A 42-year-old Caucasian female with known hypothyroidism presented to the ER with symptoms of fatigue,
nausea and abdominal discomfort of five days' duration. She denied any toxic habits or allergies, and her family
history was unremarkable. Her medications included levothyroxine 15 mcg PO daily only. Five days prior to
admission, she had completed a course of azithromycin 500 mg PO daily for five days for a respiratory tract infection.
Her physical examination disclosed stable and normal vital signs; a non-icteric patient with abdominal tenderness over
the right upper quadrant. Laboratory examination revealed AST 1382 IU/L and ALT 823 IU/L, a total bilirubin of 1.84
mg/dL, direct bilirubin of 1.14 mg/dL and ALP of 146 UI/L. An abdominal US demonstrated an increased echogenicity
of the portal triads, cholelithiasis and a dilated common bile duct of 0.83 cm in diameter. A magnetic resonance
cholangiopancreatography did not have evidence of obstructive biliary tree or acute cholecystitis. Gallstones were
present. Repeat laboratory tests (<12 hrs. apart) showed a remarkable increase of AST to 2464 IU/L, ALT to 2125
IU/L, and ALP to 210 UI/L. Coagulation panel, amylase, lipase and albumin levels remained normal. She was
transferred to the ICU with the concern for a possible evolution to fulminant hepatic failure. Supportive treatment was
provided. Hepatotoxic medications were avoided. An iron panel, TSH, infectious hepatitis serology, Cytomegalovirus,
Epstein-Barr, A1 lectin, anti-smooth muscle and anti LKM antibodies were all negative. A RUCAM (Roussel Uclaf
Causality Assessment Method) scored nine points. Liver enzymes decreased to almost half in <24 hours and bilirubin
levels normalized. Her symptoms subsided and she was transferred to regular floors. Eight days after discharge, she
was asymptomatic with near normal aminotransferase levels.
Discussion: The clinical presentation of DILI can range from transient elevation of liver enzymes to fulminant hepatic
failure. The case reflects a hepatocellular pattern of damage (ALT > 2 upper limit of normal and ALT/ALP ratio >5).
Synthetic and excreting liver functions remained in the safe range. A RUCAM score of nine is interpreted as "highly
probable" of being the causative agent.
Conclusion: Knowledge of the pattern of liver injury associated with a specific drug can be useful for diagnostic
purposes. After discontinuation of the drug, recovery is expected in the majority of patients.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Alberto Revelo : ACG Non-Member
Luis Quiel : ACG Member
Nelky Ramirez : ACG Non-Member
Jennifer Harley : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1726865
TITLE: Aneurysms and Dissections: A Case Report of an Adult Patient with Caroli's Syndrome
PRESENTER: Nancy Khov
PRESENTER (INSTITUTION ONLY): Penn State Milton S. Hershey Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Caroli's syndrome is a rare congenital disease that consists of hepatic fibrosis and multiple segmental cystic
or saccular dilatations of intrahepatic bile ducts. We present the unique case of a young male with Caroli's syndrome,
autosomal recessive polycystic kidney disease (ARPKD), and a descending aortic dissection. Our patient is a 36year-old male who was diagnosed with Caroli's syndrome and ARPKD at age three, with complications of portal
hypertension, non-bleeding esophageal varices, splenomegaly, and chronic kidney disease, stage III. He presented
with persistent bilateral flank pain and a blood pressure ranging from 113- 155/52. He was diagnosed with
hypertension in childhood, however had been off all anti-hypertensive medications for the past 15 years due to wellcontrolled blood pressures. He is a life-time nonsmoker and has no family history of liver or kidney disease. His
MELD score at time of presentation was 19 with Child-Pugh Class A. A non-contrast abdominal CT scan showed
stranding along the descending aorta near the bifurcation. A subsequent CT-angiogram revealed a type B aortic
dissection starting from the inferior renal artery origin extending into the right common iliac artery. The dissection did
not involve any viseral arteries. Other findings included a 3-cm abdominal aortic aneurysm, 1.9-cm common iliac
artery aneurysm, and 1.2-cm dilation of the celiac artery. Due to the patient's pain and non-surgical nature of the
dissection, he was started on warfarin and had subsequent resolution of his pain. Repeat imaging showed stable sizes
of his aneurysms.
There is a strong association between Caroli's syndrome and other fibropolycystic diseases, such as ARPKD. Both
Caroli's syndrome and ARPKD involve an autosomal recessive pattern of mutation in the PKHD1 genes that encodes
fibrocystin. As a result, ciliary dysfunction occurs, promoting cystogenesis. Here we report a rare case of multiple
aneurysms leading to an aortic dissection in an adult with Caroli's syndrome and associated ARPKD. This raises the
possibility of an association between adult Caroli's syndrome, ARPKD, and aneurysm formation. This area warrants
further investigation into the incidence of aneurysm formation when Caroli's syndrome and ARPKD coexist.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Nancy Khov : ACG Member
Thomas Riley : ACG Member
Ian Schreibman : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1726869
TITLE: An Atypical Appearance of Gastric Antral Vascular Ectasia (GAVE) with Complete Resolution After Liver
Transplant
PRESENTER: Nancy Khov
PRESENTER (INSTITUTION ONLY): Penn State Milton S. Hershey Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Gastric antral vascular ectasia (GAVE) is a rare cause of upper gastrointestinal bleeding in end-stage liver
patients being considered for liver transplant, and can be difficult to recognize. The correct diagnosis has therapeutic
implications for successful treatment of bleeding. A 56-year-old male with alcoholic cirrhosis, complicated by ascites
and non-bleeding gastroesophageal varices, presented for liver transplant evaluation. The most severe manifestation
of his cirrhosis was chronic blood loss anemia requiring transfusion of two units of blood every two weeks. He had
melenic stools and required frequent hospital admissions for anemia. A pre-transplant esophagogastroduodenoscopy
revealed gastroesophageal varices without stigmata of recent bleeding, diffuse GAVE in the antrum with some areas
of active oozing, and a fleshy, nodular mass in the second part of the duodenum with thick folds of oozing, friable
mucosa. The most active areas of bleeding were over this mass-like lesion. A biopsy of the mass showed vascular
ectasias with thombosis, consistent with nodular GAVE in the duodenum. The patient had treatment with serial argon
plasma coagulation, however still remained transfusion-dependent. Six months after the diagnosis of GAVE, he
underwent an orthotopic liver transplantation. After the immediate post-operative period, he was no longer transfusion
dependent. An esophagogastroduodenoscopy performed a year after his transplant showed complete resolution of his
antral GAVE, as well as complete resolution of his nodular, duodenal GAVE. The endoscopic appearances of GAVE
have been described in literature as puctate-type vascular ectasias, which are more strongly associated with cirrhosis,
as well as striped, erythematous lesions arranged radially from the pylorus, more commonly termed "watermelon
stomach." Both these presentations share the same histologic findings of mucosal capillary dilations, fibrin thrombi,
and fibromusclar hyperplasia. In our patient, we present an atypical, nodular presentation of GAVE in the duodenum.
Our case also highlights the resolution of GAVE in patients with liver disease after liver transplantation. The
recognition of GAVE is necessary for successful treatment. GAVE-induced bleeding can be treated with thermal
ablation or estrogen, and can be cured with liver transplantation; however it has not been shown to be responsive to
treatments with reduction in portal pressure.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Nancy Khov : ACG Member
Aminat Oluyemi : ACG Member
Ian Schreibman : ACG Member
Thomas Riley : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1728425
TITLE: Hemophagocytic Lymphohistiocytosis: Acute Liver Injury With A Unique Pathophysiology
PRESENTER: Katherine Shaffer
PRESENTER (INSTITUTION ONLY): Emory University
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Hemophagocytic lymphohistiocytosis (HLH) is known within the realm of pediatrics as a life-threatening
condition that may be familial or associated with autoimmune disease, viral infections, or malignancies. However, its
unique pathogenesis causes a misleading picture of abdominal pain, hepatosplenomegaly, elevated
aminotransferases, and multiorgan failure.
An 18-year-old female with no past medical history presented with one week of malaise, abdominal pain, and
shortness of breath. She was febrile, in respiratory distress, and required vasopressors. Examination was notable for
jaundice and bilateral upper quadrant abdominal tenderness. Labs were significant for pancytopenia, acute kidney
injury, bilirubin of 34, ALT of 1279, AST of 1150, INR of 3.2, fibrinogen of 88, and ferritin of 1645. MRI of the abdomen
revealed hepatosplenomegaly and hepatic edema. Extensive infectious work-up was negative, but the patient
remained febrile, on vasopressors, and high-flow oxygen, despite receiving broad spectrum antibiotics. Bone marrow
biopsy showed occasional erythrophagocytosis, not initially convincing for HLH. Thus, a trans-jugular liver biopsy was
performed, which showed kupffer cell and histiocyte hypertrophy and erythrophagocytosis, confirming the diagnosis of
HLH. The patient received dexamethasone and cyclosporine, and was weaned from vasopressors within two days.
Her symptoms and labs improved quickly, and she was discharged home with close follow-up.
HLH often presents as a non-specific constellation of acute liver injury, coagulopathy, and multi-organ system failure
with the potential for rapid fatality. Its pathophysiology is related to decreased functional perforin levels and increased
cytokines continually stimulating macrophage proliferation. This leads to a vague, yet severe, presentation, as seen in
our patient. It is important to maintain a heightened awareness for HLH because of its reversibility with corticosteroids
and cyclosporine, even at critical stages of illness.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Katherine Shaffer : ACG Non-Member
Anthony Gamboa : ACG Non-Member
Maria Delgado : ACG Non-Member
Anjana Pillai : ACG Member
John Norvell : ACG Member
Liver biopsy showing portal inflammation with bile duct injury, pericholangitis and kupffer cell and histiocyte
hypertrophy with occasional erythrophagocytosis.
IMAGE CAPTION: Liver biopsy showing portal inflammation with bile duct injury, pericholangitis and kupffer cell and
histiocyte hypertrophy with occasional erythrophagocytosis.
(no table selected)
AVERAGE SCORE: 4.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1730667
TITLE: Incarcerated Umbilical Hernia as an Immediate Complication of Large Volume Paracentesis
PRESENTER: Alexander Lalos
PRESENTER (INSTITUTION ONLY): GI consultants of NEPA
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Therapeutic paracentesis is a common procedure used in the management of refractory ascites in patients
with cirrhosis. The procedure, while generally simple and safe, has known complications such as bleeding, viscus
perforation and metabolic disturbances. We present a rare complication of therapeutic paracentesis: immediate postprocedure incarcerated umbilical hernia.
A 57-year-old woman with alcoholic cirrhosis (Child’s classification B) was admitted to ambulatory surgery unit for an
elective paracentesis. She had massive ascites and a 6-cm umbilical hernia filled with fluid. Seven liters of clear,
straw-colored fluid were removed with a 14-gauge needle, and this appeared to be a total paracentesis. She was
given 50 grams of salt-poor albumin and prepped for discharge. After standing and dressing for discharge, the patient
developed abdominal pain and distension. On examination, it was obvious that she had gas-filled bowel loops in a
hernia that could not be reduced (figure). Abdomen was tympanic, consistent with bowel obstruction. Surgical consult
was obtained and she underwent reduction and repair of the umbilical hernia, which she tolerated well.
Elective repair of umbilical hernias in patients with cirrhosis is usually frowned upon, as hernia recurrence is common
unless the ascites can be controlled with diuretics. In addition, this patient group is generally a poor surgical risk due
to infection, bleeding and poor wound healing. However, there was not an option in this case, as the hernia presented
acutely. Incarceration can occur due to a decrease in tension in the umbilical ring following large volume paracentesis.
It may be reasonable to consider TIPS in patients with a significant umbilical hernia whose ascites cannot be
controlled with diuretics and whose hernia size runs a risk of incarceration. At the very least, clinicians should be
aware of this complication and evaluate patients complaining of pain and distention after paracentesis to rule out this
life-threatening condition and be prepared to act quickly to avoid poor outcomes in this compromised group of
patients.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Alexander Lalos : ACG Member
JayaKrishna Chintanaboina : ACG Member
IMAGE CAPTION:
(no table selected)
AVERAGE SCORE: 4
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1730733
TITLE: Acute Liver Failure Following a Year of Consumption of a Popular Sugar-Free Energy Drink
PRESENTER: Brian Huang
PRESENTER (INSTITUTION ONLY): Department of Medicine, Cedars Sinai Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 36-year-old Caucasian male without prior medical history initially presented to another facility with one
week of right upper quadrant (RUQ) abdominal pain, jaundice and fatigue. After abnormal lab values (Table 1) were
found, he left that facility and presented to this hospital. He admitted to weekend binge drinking and drank 10 beers
three hours prior to symptom onset. He denied taking herbal remedies, homeopathic medications or other
supplements. He drank up to three energy drinks (Figure 1) on a daily basis for the past year.
Physical exam showed stable vital signs, jaundice, spider nevi and RUQ tenderness. Initial work-up was negative for
viral, ischemic or autoimmune hepatitis. On HD #6, a liver biopsy showed severe active hepatitis with bridging
necrosis consistent with an herbal/drug-toxicity pattern. On HD #9, the patient was discharged home, but was soon readmitted for worsening LFTs. With an INR of 4.2, he was placed on the UNOS waiting list with a MELD score of 41.
On HD #14 of this 2nd hospitalization, a suitable donor became available and the patient underwent successful liver
transplantation. Gross liver pathology showed massive hepatocellular necrosis and parenchymal collapse consistent
with drug-induced liver injury. He was discharged on post-operative day number seven.
Discussion: A similar case report by Vivekanandarajah et al. described a young woman who drank 10 cans of an
energy drink for two weeks, resulting in acute hepatitis. The authors concluded that Vitamin B3 (niacin) was the culprit
ingredient.
Our case report details a patient who drank a sugar-free energy drink over a longer period and had a more serious
clinical course. The patient’s prior alcohol use may have provided a “first hit” on the liver, making it more susceptible to
further insults. The energy drink in this case report contains many ingredients, some of which do not have a wellestablished safety profile. While drinking modest amounts of energy drinks appears to be relatively safe, frequent
consumption over an extended period of time has recently been linked with hepatic injury.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Brian Huang : ACG Member
David Kunkel : ACG Non-Member
Mohamed El Kabany : ACG Member
Figure 1: Ingredients of Sugar Free Energy Drink
IMAGE CAPTION: Figure 1: Ingredients of Sugar Free Energy Drink
Table 1: Laboratory Findings
Variable
Reference
OSH (8 days
1st
2nd
Discharge/
Range
prior to 1st
Admission
Admission
Post-Op Day
admission)
WBC
4.16-9.95
6
4.3
3.6
4
7.5
15.6
14.5
15.3
11.8
185
159
207
113
-
1
1.3
0.6
1000/uL
Hemoglobin
13.5-17.1
G/DL
Platelets
143-398
1000/UL
Creatinine
0.5-1.3
MG/DL
AST
7-36 U/L
1541
2253
1250
26
ALT
4-45 U/L
2995
2432
1004
114
Alkaline
31-103 U/L
231
183
116
66
Total
0.2-1.1
16.1
15.6
23.1
3.4
Bilirubin
MG/DL
INR
N/A
1
1.6
3.7
1.1
Phosphatase
TABLE TITLE: Table 1: Laboratory Findings
AVERAGE SCORE: 4.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1731181
TITLE: Acute Liver Failure with Hepatitis E and Epstein-Barr Virus Co-Infection
PRESENTER: Joshua Peck
PRESENTER (INSTITUTION ONLY): The Ohio State University Wexner Medical Center/Nationwide Children's
Hospital
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 20-year old female pig-farmer without significant medical history presented with three days of abdominal
pain, vomiting, fevers and confusion. Upon arrival, she was febrile to 101.5 F; remaining vital signs were stable. She
was disoriented and drowsy. Physical exam was notable for scleral icterus, asterixis, bilateral basilar crackles and a
diffusely tender abdomen. Labs were remarkable for total bilirubin 6.8, direct bilirubin 4.1, alkaline phosphatase 203,
ALT 107, AST 103, INR 2.8 and WBC 13,500. A comprehensive infectious panel was notable for a positive Hepatitis E
Virus (HEV) IgM antibody, negative HEV IgG, and positive EBV IgG antibody with viral load of 37,632. An autoimmune
panel, including ANA, liver-kidney microsomal antibody and anti-mitochondrial antibody was negative. The serum
acetaminophen level was <10 and serum heavy metal and urine drug screens were negative. She was empirically
started on N-acetylcysteine, vancomycin, piperacillin/tazobactam and acyclovir.
Shortly after admission, the patient became progressively somnolent with increasing oxygen requirements, prompting
a transfer to the intensive care unit (ICU). She soon developed complete heart-block requiring a temporary
pacemaker. A transesophageal echocardiogram was unremarkable, but a cardiac MRI demonstrated myocarditis.
After five days being paced, her intrinsic rhythm returned, and she no longer required pacing. Her mentation improved,
and she was transferred out of the ICU. Upon drastic clinical improvement and resolution of the liver failure, she was
discharged home with the following labs: total bilirubin 1.2, direct bilirubin 0.6, AST 54, ALT 43, alkaline phosphatase
247 and INR 1.1.
Discussion: The typical presentation of acute HEV infection typically resembles that of other viral hepatitis with fever,
abdominal pain, jaundice and constitutional symptoms, with acute liver failure being a less-common phenomenon.
EBV is often asymptomatic, with mild self-limited hepatitis reported in 80 to 90% of cases. Less common
complications include hemolytic anemia, aplastic anemia and myocarditis. Fulminant hepatitis is a very rare
complication, and has an overall mortality of 90%.
Our case demonstrates a co-presentation of two viruses which are each known to cause acute liver failure. It is
possible that two bad infections at the same time wreaked havoc on her organs. Another possibility is that HEV was
responsible for all the symptoms and the EBV was an epiphenomenon. We believe that the myocarditis was likely
from EBV, which led to heart block. Regardless of the exact mechanism of disease, it is important for physicians to
keep a broad differential diagnosis when presented with fulminant hepatic failure.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Joshua Peck : ACG Non-Member
Lana Alghothani : ACG Non-Member
Steven Campbell : ACG Non-Member
John Davis : ACG Non-Member
James Hanje : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1731656
TITLE: TIPS to Treat Gross Hematuria
PRESENTER: George Saffouri
PRESENTER (INSTITUTION ONLY): Mayo Clinic
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Purpose: The most common site of bleeding in patients with portal hypertension is gastro-esophageal
varices. Bleeding from sites other than gastro-esophageal varices is termed ectopic variceal bleeding. Here, we
present a patient with ectopic urinary bladder varices secondary to portal hypertension, who presented with hematuria
and symptomatic anemia.
Case: A 52 year-old man with alcoholic cirrhosis was admitted with painless gross hematuria and anemia requiring six
units of packed RBCs. Pertinent medical history included portal hypertension with known esophageal and rectal
varices, as well as an appendectomy 25 years prior. A cystoscopy demonstrated generalized bladder neck mucosal
oozing of blood requiring fulguration. The patient, however, continued to have intermittent, transfusion-dependent
hematuria over several months. Review of a previous CT revealed extensive abdominal/pelvic varices surrounding the
urinary bladder. A second cystoscopy revealed significant friable venous dilatation throughout the bladder mucosa
consistent with ectopic varices from portal hypertension. The decision was made to place a transjugular intrahepatic
portosystemic shunt (TIPS) to decompress the portal system and bladder varices. Following TIPS, the hematuria
completely resolved. Six months later the patient went on to liver transplantation and is currently doing well.
Discussion: This case demonstrates an uncommon etiology of symptomatic anemia and gross hematuria from urinary
bladder varices due to portal hypertension. Indeed, reports of bleeding bladder varices appear in only a handful of
cases in the literature. Ectopic varices are portosystemic shunts that can occur anywhere in the GI tract. Intraabdominal surgery with subsequent adhesions can impede the normal port-systemic anatomy, forming unusual
collateral routes. This is the purported mechanism of bladder variceal formation, which is consistent with the patient’s
history of appendectomy. Treatment of ectopic varices depends on the clinical scenario, but can range from variceal
embolization to beta blockade. With a patent portal vein, TIPS can successfully control bleeding via portal
decompression, as was performed in this case. In any patient with portal hypertension, it is important to consider the
possibility of ectopic varices in the presenceof unexplained visceral bleeding.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
George Saffouri : ACG Non-Member
Nataliya Razumilava : ACG Non-Member
Matthew Gettman : ACG Non-Member
Patrick Kamath : ACG Non-Member
Bladder varices on CT abdomen/pelvis (red arrow)
IMAGE CAPTION: Bladder varices on CT abdomen/pelvis (red arrow)
(no table selected)
AVERAGE SCORE: 3.5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1731796
TITLE: Long-acting Octreotide for the Prevention of Recurrent Variceal Bleeding was Well- Tolerated and Appeared
Effective
PRESENTER: Christian Speer
PRESENTER (INSTITUTION ONLY): Northwest Permanente
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: We describe the use of long-acting octreotide in a cirrhotic patient with recurrent variceal bleeding deemed
too frail for TIPS, and ineligible for transplantation.
A 36-year-old woman with decompensated alcoholic cirrhosis (Child Pugh >12, MELD >25) was ineligible for liver
transplantation. She was cachectic, with a BMI of 18, had medically-controlled hepatic encephalopathy, diureticresistant ascites, and a recent history of SBP. She also had recurrent variceal bleeding with increasing frequency,
despite treatment with non-selective beta blockers (NSBB) and repeated endoscopic variceal ligation (EVL). It was
obvious that standard therapy was inadequate for the prevention of variceal bleeding. Deemed too frail for TIPS, longacting octreotide 200 mcg SC tid was started as VI octreotide was stopped. After two days without complications,
subcutaneous octreotide was switched to a single dose of long-acting octreotide 10 mg IM without local or systemic
complications (INR=2.7), and repeated four weeks later. All other treatments, including NSBB, were continued. There
was no adverse effect on renal or hepatic function, mental status, or general well-being. She was discharged home
five days later. She was readmitted 12 days later with anemia, though there had been no overt bleeding. The next
day, an EGD showed the known varices, but there were no red wale signs or stigmata of recent bleeding, and there
was no blood in the stomach. She survived another two weeks without bleeding.
Addition of long-acting octerotide to NSBB and EVL was well-tolerated in our severely ill patient, and it appeared
effective. When treated with conventional therapy, there was recurrent bleeding up to every two weeks prior to use of
long-acting octreotide, following which she survived 33 days without variceal bleeding and had an improved quality of
life.
Regular octreotide is an established and effective treatment for acute variceal bleeding. Long-acting octreotide is an
established and effective treatment for symptomatic neuroendocrine tumors. However, data on the use of long-acting
octreotide for variceal bleeding is regrettably sparse. Long-acting octreotide might provide clinical benefits and
improve quality of life in select patients with portal hypertension who have failed medical treatment and cannot benefit
from OLT or TIPS.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: Yes
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Christian Speer : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1732259
TITLE: A Curious Case of Isolated Hepatic Artery Thrombosis Leading to Multiple Liver Infarcts in a Non-transplant
Patient
PRESENTER: Tarek Almouradi
PRESENTER (INSTITUTION ONLY): John H. Stroger hospital
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction: Spontaneous hepatic artery thrombosis is an extremely rare disorder with only few cases
reported in literature.
Case presentation: A 62-year-old female with multiple medical problems, including breast cancer, presented to the
emergency department with five days of right upper quadrant pain, nausea and vomiting. Her physical exam was
remarkable for right upper quadrant tenderness to palpation, but no guarding or rebound tenderness.
Her initial laboratory work was significant for abnormal liver function tests, mainly aspartate aminotransferase, alanine
aminotransferase (745 and 431 U/L respectively), compared to normal levels on a routine blood work done two days
prior to admission.
A computed tomography with administration of oral and intravenous contrast showed a thrombus within the hepatic
artery with multiple hepatic infarcts; no portal vein thrombosis was noted.
Workup for chronic liver disease along with hypercoagulability was negative.
Over the following few days, AST and ALT levels continued to rise up to 2065 and 1217 U/L respectively on day five,
and started to trend down after.
Discussion: Hepatic infarcts following hepatic artery compromise are very rare because of the dual blood supply from
the portal vein and the hepatic artery, along with the extensive hepatic arterial collateral system.
The vast majority of cases of hepatic artery thrombosis are reported as complications of orthotopic liver
transplantation; it also complicates various procedures, such as placement of hepatic catheters/Port systems for
intraarterial chemotherapy of liver tumors, and hepatic artery reconstruction following ablative surgery for hepatobiliary
and pancreatic malignancies.
We believe that our case is unique because of two reasons: 1.) Our patient did not undergo any procedure that may
have precipitated hepatic artery thrombosis. 2.) Despite the absence of concurrent portal vein thrombosis, she had
biochemical and imaging findings of hepatic ischemia.
Methods: NA
Results: NA
Conclusion: NA
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Tarek Almouradi : ACG Member
William Riles : ACG Member
Bashar Attar : ACG Member
IMAGE CAPTION:
Liver function tests
Test
Two days prior
At presentation
Peak value
to admission
Reference
range
Albumin
4.00
3.8
NA
3.8-5.2
Total bilirubin
0.6
0.9
1.3
0.2-1.2
AST
22
745
2065
0-40
ALT
25
431
1217
5-35
ALP
135
174
486
50-120
GGT
159
181
256
3-60
LDH
181
300
2283
85-210
AST: Aspartate aminotransferase
ALT: Alanine aminotransferase
ALP: Alkaline phosphatase
GGT: Gamma glutamil transferase
LDH: Lactate dehydrogenase
TABLE TITLE: Liver function tests
AVERAGE SCORE: 4.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1732294
TITLE: Post-Infantile Giant Cell Hepatitis in the Setting of Drug-Induced Liver Injury and Latent Syphilis
PRESENTER: Christopher Mulder
PRESENTER (INSTITUTION ONLY): San Antonio Military Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction: Giant cell hepatitis is a common presentation of liver disease in neonates, but a rare entity in
adults, accounting for 0.1-0.25% of liver disease in adults. Post-infantile giant cell (PIGCH) or syncytial-cell hepatitis is
often characterized by multinucleated giant cells on liver biopsy and a fulminate hepatitis, which may require
orthotropic liver transplant. There are many reported causes; however, there is often no cause is found. The most
commonly reported etiology is autoimmune hepatitis. Other less common causes include herbal remedies,
medications, and infections. PIGCH is a descriptive histologic diagnosis; therefore, determination of the cause is the
key to treatment. We report a case of PIGCH due to the combination of M-drol, a testosterone analogue taken as a
weight-building supplement, and latent syphilis.
Case Report: A 36-year-old male presented with jaundice two weeks after starting a testosterone analogue. He
discontinued the supplement, but his jaundice persisted and his bilirubin continued to rise over the ensuing weeks.
Serologic testing was negative for hepatitis A, B, C, and E, CMV, EBV, HSV, and HIV. Evaluation for autoimmune
hepatitis was negative for anti-smooth muscle and anti-nuclear antibodies. His bilirubin continued to climb to 44.5
mg/dL. ALT was 290U/L, AST 220U/L, and alkaline phosphatase 359U/L. MRCP was negative for obstruction. Liver
biopsy revealed giant cell transformation of numerous hepatocytes and cholestatic hepatitis. After two months of
persistent bilirubin >30mg/dL, his hepatic synthetic function and renal function began to decline. He was listed for liver
transplant with a MELD of 26. An RPR was positive, but physical findings of syphilis were absent. Treponemal
pallidum hemaglutination assays confirmed the diagnosis of latent syphilis. He was started on penicillin treatment with
rapid improvement of bilirubin, creatinine, and hepatic synthetic function, all of which eventually normalized.
Discussion: PIGCH is a severe form of hepatitis that has several different potential etiologies, two of which were
present in this patient: androgenic supplements and infection. Syphilis has been reported to cause infantile giant cell
hepatitis, but is a previously unreported cause of giant cell hepatitis in adults. We suspect the testosterone analogue
contributed to the hepatitis, and may have been the inciting event, but the resolution of liver injury correlating with the
treatment of the latent syphilis supports syphilis as the cause of the persistent liver injury. This case highlights syphilis
as an unusual, but treatable, cause of giant cell hepatitis. Testing for syphilis should be considered in any persistent
liver injury.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Christopher Mulder : ACG Member
James Francis : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 2.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1733303
TITLE: Primary Herpes Esophagitis in a Liver Transplant Recipient
PRESENTER: Chau Che
PRESENTER (INSTITUTION ONLY): New York Medical College
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Herpes esophagitis is a common infection in immunocompromised patients. It is usually due to secondary
reactivation, but it may also present as a primary infection. We present a case of primary infection of herpes simplex
virus in a liver transplant recipient.
Case: A 27-year-old woman with a history of liver transplant for autoimmune hepatitis-induced cirrhosis underwent a
change of medication from tacrolimus to sirolimus, due to chronic kidney disease from a calcineurin inhibitor. Within
one week, the patient developed fevers, myalgias, and odynophagia. Prior to transplant, she had negative testing for
cytomegalovirus (CMV), IgG Ab, and herpes simplex virus (HSV) type 1 and 2 IgG Ab. Physical exam showed
temperature of 102.3°F, multiple shallow ulcers on the tongue and posterior pharynx, and no hepatosplenomegaly or
lymphadenopathy. Laboratory tests showed white blood cell count of 4,100 cells/mm3, hemoglobin 11.5 g/dL,
hematocrit 35.7%, platelet count 167,000 cells/mm3, creatinine 1.85 mg/dL (baseline 1.5 mg/dL), sirolimus trough 5.7
μg/L and normal liver chemistries. CMV PCR, EBV PCR, and HIV Ab were negative. The ulcers from the oropharynx
were sampled; cultures were positive for HSV. An upper endoscopy showed exudates at the gastroesophageal
junction with no ulcers. Esophageal biopsies showed numerous HSV-infected squamous cells. HSV-associated
erosive esophagitis was confirmed by immunostaining. Serum HSV-1 IgM Ab was positive, confirming a primary
herpes infection causing esophagitis. HSV-2 IgM Ab was negative. The patient was started on acyclovir with
improvement of her symptoms, and discharged home on valacyclovir.
Discussion: The esophagus is the visceral organ most commonly affected by herpes, although it is not uncommon to
have concurrent oral lesions. Herpes esophagitis is most commonly found in the immunocompromised patient,
especially bone marrow and solid organ transplant patients. The vast majority of cases are caused by HSV-1. The
typical findings found endoscopically are well-circumscribed ulcers that have a “volcano-like” appearance. However,
exudates and plaques may be the only findings endoscopically. Biopsies and/or brushings should be taken from
exudative areas and the edge of ulcers, where the virus that infects the squamous epithelium are most likely to be
present. Oral acyclovir is recommended as therapy in the immunocompromised patient. If symptoms are severe,
intravenous acyclovir may also be used. Viscous lidocaine provides only modest symptomatic benefit. Opportunistic
infections, including HSV, should always be considered in immunocompromised patients who present with fever. This
is particularly the case in patients with oral lesions or esophageal complaints.
Methods: NA
Results: NA
Conclusion: NA
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Chau Che : ACG Member
Roxana Bodin : ACG Non-Member
David Wolf : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 5.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: Important teaching point that immunosuppression can predispose to new/primary HSV|Julia
LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego: [No Comments]
CONTROL ID: 1733347
TITLE: Time to Consider Empiric Acyclovir
PRESENTER: Amit Aravapalli
PRESENTER (INSTITUTION ONLY): Carolinas Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 63-year-old female presented to the emergency department with a two-day history of fever of 101.9°F and
worsening fatigue. She denied a history of liver disease and was otherwise in good health, aside from a history of
arthritis. She denied any recent changes in medications, use of antibiotics or travel history. Urine toxicology screen,
acetaminophen level and hepatitis A-C serology were negative. Her laboratory assessment was notable for AST 4755
IU/L, ALT 3569 IU/L and an INR of 1.4. She was admitted into her local hospital and started on intravenous Nacetylcysteine. Overnight, she developed subtle changes in behavior without any change in level of consciousness.
She was subsequently transferred to a liver transplant center.
Upon arrival, the patient was oriented, but very somnolent, and remained febrile at 103.1°F. Physical exam was
negative for stigmata of chronic liver disease, rash or asterixis. Laboratory assessment revealed total bilirubin 0.6
mg/dl, AST 7392 IU/L, ALT 5942 IU/L, INR of 2.2, WBC 2900 cells/ mm3, hemoglobin 16 g/dL and platelets of
29,000/mm3. Abdominal ultrasound showed a normal-appearing liver with normal hepatic and portal flow. Further
history from family revealed the patient was taking oral prednisone the past few weeks for chronic joint pain. Given
this history, combined with fever, leukopenia and anicteric hepatitis, she was started on empiric IV acyclovir for
possible herpes simplex virus (HSV)-induced liver failure. She underwent expedited liver transplant evaluation. A
trans-jugular liver biopsy revealed minimal inflammation with scattered hepatocyptes with glassy nuclear inclusions,
azonal areas of necrosis and positive HSV stain. Her serum HSV DNA testing by PCR was 1.2 x 10^6 copies/ml,
although her initial HSV IgM was within reference range. Her laboratory values normalized completely within 15 days,
and she was discharged to a local rehab center.
HSV-induced liver failure accounts for only 1% of all ALF, but confers a mortality rate of 75%. Although
immunocompetent patients can be affected, 75% of affected patients are immunosuppressed or pregnant in the third
trimester. Patients who present with fever, vesicular skin lesions, leukopenia and anicteric hepatitis need to be
considered for empiric acyclovir therapy and transferred to a liver transplant center. Serological testing with antibodies
against HSV in the serum is nonspecific and has low utility in early treatment decisions. Confirmation of diagnosis is
best performed with liver biopsy and serum HSV PCR. Empiric therapy with acyclovir for patients at risk may obviate
the need for liver transplantation.
Methods: na
Results: na
Conclusion: na
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Amit Aravapalli : ACG Member
Mike Ryan : ACG Non-Member
Ross Jones : ACG Non-Member
Mark Russo : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3.5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1733968
TITLE: Vanishing Bile Duct Syndrome: A Rare Cause of Cholestasis in Hodgkin's Lymphoma
PRESENTER: Mariajose Rojas De Leon
PRESENTER (INSTITUTION ONLY): John H. Stroger Jr. Hospital of Cook County, Department of Gastroenterology
and Hepatology
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Case: A 46 year-old Hispanic male presented with a 3-day history of jaundice, poor appetite, and abdominal
pain. Past medical history was unremarkable, and the patient was not taking medications, illicit drugs, or alcohol. He
denied B symptoms. Physical exam was unremarkable except for jaundice; no stigmata of chronic liver disease.
Investigations showed total bilirubin of 14.2 mg/dL (direct 9mg/dL), GGT 362, AP 581, AST 120, ALT 248, albumin
4.1g/dL. Serology was negative for HIV, hepatitis A, B and C. CT showed normal liver without intra or extra-hepatic
duct dilatation, and multiple large para-aortic and peri-hepatic lymph nodes (LN). Biopsy of a LN showed mixed
cellularity Hodgkin lymphoma (HL), stage I/II. Bilirubin continued to rise to 27.2 mg/dL, and despite two cycles of
chemotherapy with doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD), bilirubin increased to 41 g/dL, which
lead to ABVD cessation and initiation of radiotherapy (RT) to the abdomen. An ERCP was normal. A liver biopsy
showed marked canalicular and focal hepatocytic cholestasis, minimal inflammation, and ductopenia; no malignant
cells, steatosis or iron deposition were seen, and a diagnosis of vanishing bile duct dyndrome (VBDS) as the cause of
cholestasis was established. Ursodeoxycholic acid was started, RT was completed, and ABVD was restarted when
bilirrubin decreased. Treatment was completed and a follow-up CT showed a decrease of LN size, and a PET scan
was negative. Currently,18 months after diagnosis, the patient remains well and in remission. His bilirubin has
normalized, and LFT have improved to near normal.
Discussion: Cholestasis as the presenting symptom of HL is very uncommon (<4%). It can be caused by
lymphomatous infiltration of the liver, extrahepatic biliary obstruction by lymphadenopathy, concurrent viral infections,
or drug toxicities. Rarely, it can be due to a paraneoplastic phenomenon, which can be divided into VBDS and pure
intrahepatic cholestasis without ductopenia. The pathophysiology of VBDS is unknown, but is thought to be caused by
release of toxic cytokines from lymphoma cells, leading to destruction of bile ducts without significant inflammation.
Diagnosed by exclusion and supported by histology in the absence of liver involvement by HL. VBDS is rare, and
usually fatal. Only 18 cases of VBDS have been reported since its description in 1993. The overall mortality is 65%,
liver failure being the leading cause, followed by sepsis and recurrence of HL. However, 30% of cases have normal
LFT without recurrence at 24 months. There is no difference in outcome across sex, age, type of HL, B-symptoms, or
chemotherapy or steroids, but those who are stage I/II at presentation and receive radiotherapy appear to have a
better outcome.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Mariajose Rojas De Leon : ACG Member
Yohannes Bayissa : ACG Non-Member
Pramoda Koduru : ACG Non-Member
Sylvia Velinova : ACG Non-Member
Carol Czapar : ACG Non-Member
Gijo Vettiankal : ACG Member
Bashar Attar : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1734035
TITLE: Fulminant Hepatic Failure in a Patient with Hemophagocytic Syndrome
PRESENTER: Deepak Venkat
PRESENTER (INSTITUTION ONLY): University Hospital/Case Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 55-year-old male presented with two months of jaundice and fevers. Past medical history was
unremarkable. Social history revealed daily heavy whiskey consumption. Family history revealed primary sclerosing
cholangitis (PSC). Lab data also revealed significant pancytopenia. Serologic evaluation for other causes of liver
disease and hepatic imaging evaluation were grossly unremarkable. Liver biopsy was read as consistent with
alcoholic hepatitis. The patient was treated with steroids, with improvement in his clinical parameters. The patient was
readmitted 6 weeks later with fevers and worsening jaundice, despite alcohol abstinence and compliance with
steroids. Exam revealed jaundice, hepatomegaly, asterixis and anasarca. Lab data revealed bilirubin 14, direct
bilirubin, alkaline phosphatase 608, ALT 510, AST 230, creatinine 5.2, WBC 1.5, hemoglobin 4.7, platelets 16,000,
and INR 1.5. Infectious work-up was negative. Bone marrow biopsy revealed a hypercellular marrow without clonal
proliferation. Frequent blood product transfusions and dialysis were required. He was then transferred to our
institution. Given ALT>AST and apparent consumptive process causing pancytopenia, alcoholic hepatitis was not felt
to be the underlying diagnosis. Review of the prior liver biopsy was not consistent with alcoholic hepatitis. Additional
labs revealed ferritin 40,000, and EBV PCR>1000 copies. Repeat bone marrow biopsy was consistent with natural
killer cell lymphoma with ongoing hemophagocytosis. He was started on chemotherapy, but deteriorated and expired
three days later.
Hemophagocytic syndrome involves phagocytosis of erythrocytes, leukocytes, platelets and their precursors in the
bone marrow and peripheral tissues. The process is typically driven by atypical infections, malignancy or autoimmune
disease. Typical findings include markedly elevated ferritin, fevers, splenomegaly, hypertriglyceridemia,
hypofibrinogenemia, hepatitis, and demonstration of hemophagocytosis. Of note, nearly 20% of bone marrow biopsies
fail to show hemophagocytosis, and multiple biopsies may be required. Liver involvement is noted in approximately
80% of cases. Biopsy may reveal kupffer cell hyperplasia, sinusoidal dilation and occasionally tissue
hemophagocytosis. Overall mortality is approximately 100% in those with underlying hematologic malignancy.
Our case highlights a few important points: First, ALT>AST and severe consumptive pancytopenia are not typically
seen in alcoholic hepatitis. Second, a markedly elevated ferritin (40,000 in this case) in the presence of elevated LFT’s
and significantly deranged hematologic parameters should prompt consideration of a diagnosis of hemophagocytic
syndrome.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Deepak Venkat : ACG Member
Stanley Cohen : ACG Member
Badar Muneer : ACG Non-Member
Anthony Post : ACG Member
Pierre Gholam : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 2.5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1734049
TITLE: Inflammatory Pseudotumor Containing Kayexalate Crystals: A Case Report and Review of the Literature
PRESENTER: Matthew Soape
PRESENTER (INSTITUTION ONLY): Texas Tech University Health Sciences Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction: Kayexalate or sodium polystyrene sulfonate has long been used for the treatment of
hyperkalemia. Inflammatory pseudotumor (IP) is a benign inflammatory mass, and occurs secondary to infection or
foreign body. We present a case of an extra-intestinal IP containing Kayexalate crystals.
Case Report: A 62-year-old woman with history of type II DM and CKD presented with abdominal pain. Surgical
history included a partial colectomy with colostomy for diverticulosis. Her medication regiment included Kayexalate.
She was febrile upon presentation, and had tenderness over the right side of the abdomen. A CT scan revealed a
mass below the liver and near the ostomy(Fig 1A). She was started on antibiotics and underwent surgical evacuation
of the mass, with cultures positive for E. coli. A repeat CT scan showed a residual mass in the same location, but
smaller in size. Biopsy of the mass showed spindle and stellate cells mixed with histiocytes and inflammatory cells.
Occasional polygonal crystals with a “fish scale” appearance were found (Fig 1B). The crystals were highlighted by
PAS stains.
Discussion: Kayexalate is used to treat hyperkalemia, promoting excretion of potassium ions into the intestine. It is
often administered with sorbitol to prevent impaction. Sorbitol has been known to cause intestinal necrosis, resulting in
mild GI bleeding to perforation. Sorbitol-induced intestinal necrosis is thought to be from increased prostaglandin
activity and vasospasm. Identification of Kayexalate crystals is considered the hallmark of Kayexalate toxicity. These
crystals have a polygonal and “fish scale” appearance that display a red color on PAS stains. IP is often considered to
be a benign mass, and composed of spindled myofibroblasts set in dense collagen and inflammatory cells. Their
etiology is thought to be a reactive process in response to infection or foreign body. Our patient developed ischemic
colitis, which is found in previously-reported cases of GI complications to Kayexalate, and formed an abscess.
Following evacuation, the abscess likely evolved into an IP. We hypothesize the IP is attributed to an infectious
etiology, with the Kayexalate crystals coming to reside in the lesion, consistent with other case reports. Regardless,
the presence of Kayexalate in this case is unique in its location and association with an IP.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Ryan Romano : ACG Non-Member
Seshadri Thirumala : ACG Non-Member
Matthew Soape : ACG Non-Member
Walter Cushman : ACG Non-Member
Fig 1. A) CT Abd with mass in the RLQ. B) Polygonal crystals with “fish scale” appearance.
IMAGE CAPTION: Fig 1. A) CT Abd with mass in the RLQ. B) Polygonal crystals with “fish scale” appearance.
(no table selected)
AVERAGE SCORE: 3.5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1734052
TITLE: Acute Liver and Multi-Organ Failure Secondary to Intentional Iron Overdose
PRESENTER: Kirk Russ
PRESENTER (INSTITUTION ONLY): UAB Department of Internal Medicine
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction: Intentional iron overdoses are rare in adults, but have severe consequences. We report two
patients with multi-organ system failure occurring rapidly after large quantity oral iron ingestions.
Case Discussion: A 26-year-old woman was transferred from an outside hospital (OSH) for acute liver failure (ALF):
48 hours prior, she had intentionally ingested a large amount of iron supplements. At initial presentation, she had
nausea, gastrointestinal bleeding and normal liver enzyme levels. She then developed abdominal pain, tender
hepatomegaly, elevated liver enzymes and coagulopathy (see table). No asterixis or encephalopathy was present.
Deferoxamine, N-acetylcysteine (NAC) and dialysis were initiated. She progressed to coma, shock, brainstem
herniation and death.
Case B: A 35-year-old woman with prior gastric bypass surgery, hypertension, iron deficiency anemia and previous
suicide attempt was transferred from an OSH with ALF after intentionally ingesting 300 iron pills the evening before.
She developed nausea, vomiting, diarrhea and abdominal pain. Initially, she was hypertensive, had a tender
abdomen, but no asterixis. Acute kidney injury (AKI) and severe acidosis were managed with intravenous fluids and,
eventually, dialysis. She also received a proton pump inhibitor, NAC, polyethylene glycol laxative and deferoxamine.
She recovered after 16 days, with liver enzymes and INR near normal. However, she remained dialysis-dependent on
discharge, and subsequently has been lost to follow up. Acetaminophen adducts were negative, and no radio-opaque
pills were identified on abdominal x-ray (KUB) in either case.
Discussion: Iron overdose causes rapid onset multi-organ failure with high mortality. Iron-induced oxidative damage
results from hepatocyte exposure to high quantities of non-transferrin bound iron via the portal venous system,
resulting in excessive free radical production. Peak serum iron levels occur 4-6 hours after ingestion. Bowel irrigation
is indicated if tablets are identified on KUB. IV deferoxamine should be administered early if systemic signs such as
metabolic acidosis are present. NAC can be given empirically. AKI is thought to be from direct mitochondrial injury and
lactic acidosis. In case B, survival may, in part, have been due to the history of gastric bypass surgery, which may
have limited absorption.
These patients were enrolled in the Acute Liver Failure Study Group registry, supported by U-01-58369-014 from
NIDDK.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: Yes
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Kirk Russ : ACG Non-Member
Ali Khan : ACG Member
Laura James : ACG Non-Member
Michael Schilsky : ACG Non-Member
Oren Fix : ACG Member
William Lee : ACG Member
Brendan McGuire : ACG Member
(No Image Selected)
Case
Age
Peak
Peak
Peak
Peak
Peak
Peak
Peak
Peak
INR
Bilirubi
AST
ALT
Lactat
Creati
iron
ferritin
n
(U/L)
(U/L)
e
nine
(μMol/
(ng/dL)
(mg/dL
(mmol/
(mg/dL
L)
)
L)
)
A
26
>12
4.3
8249
7655
18.5
3.92
830
4525
B
35
3.8
17.7
3698
3368
6.9
10.7
7247
599
TABLE TITLE:
AVERAGE SCORE: 3.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1734119
TITLE: Spontaneous Splenic Rupture: First Presentation of Alcoholic Steatohepatitis
PRESENTER: Sweta Kochhar
PRESENTER (INSTITUTION ONLY): UAMS
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Case Report: A 56-year-old Caucasian woman with history of moderate alcohol intake presented with
sudden-onset, severe abdominal pain with nausea and dizziness for a few hours. On examination, she was afebrile,
hypotensive, tachycardic, and icteric. There were multiple spider angiomata over the chest. She had tenderness and
guarding in the epigastrium and left upper quadrant without rigidity. Rectal vault had brown stool that was guaiac
negative. Lab data were: hemoglobin 7.6 mg/dL (down from 14 mg/dL six months ago); platelet 238,000/µL; total
bilirubin 7.7 mg/dL; AST 135 IU/L; albumin 2.6 g/dL; and INR 1.3. CT abdomen showed an enlarged echogenic liver
and a normal-appearing pancreas. Spleen had a rupture postero-inferiorly with resultant perisplenic hematoma. After
taking resuscitative measures, an urgent exploratory laparotomy showed splenic rupture in multiple pieces, still
connected to the hilum with massive hemoperitoneum of 1.5 L and hepatomegaly. A splenectomy and wedge liver
biopsy was done. Liver histopathology showed extensive steatosis (80-90%), ballooning degeneration, severe
cholestasis, Mallory-hyaline, and mixed inflammatory infiltrate. Trichrome stain highlighted extensive sinusoidal and
portal fibrosis with focal areas of bridging fibrosis. Splenic histopathology showed capsular disruption with subcapsular
and intraparenchymal hemorrhage, and acute inflammation. Etiological work-up for liver disease and splenic rupture
including serum copper, viral panel, hemochromatosis screen, alpha-1 antitrypsin, autoimmune panel, monospot,
leukemia, and lymphoma panel was negative. Cause of her splenic rupture was felt to be related to portal
hypertension from alcoholic steatohepatitis and early cirrhosis.
Discussion: Non-traumatic splenic rupture (NSR) is a rare, but life threatening condition. Diagnosis is often suspected
based on clinical symptoms. Paracentesis with aspiration of fresh blood is useful to diagnose intraperitoneal
hemorrhage. Abdominal ultrasound is especially useful in hemodynamically unstable patients. CT can shows grade of
splenic damage severity and intraperitoneal free fluid. In a review of 845 cases of NSR, the spleen was normal in 7%.
The major pathologic etiological groups were neoplastic (30%), infectious (27%), and inflammatory (20%). In our
patient, we ascribed the splenic rupture to congestion resulting from steatohepatitis. This patient had patent portal and
splenic vein, ruling out congestion due to thrombosis. This is a unique case for rarity of atraumatic splenic rupture as
presenting manifestation of steatohepatitis with early changes of bridging fibrosis.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Sweta Kochhar : ACG Member
Nitin Relia : ACG Non-Member
Abhishek Agarwal : ACG Non-Member
Farshad Aduli : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1734256
TITLE: Fibrolamellar Carcinoma of the Liver with Vertebral Metastasis: A Rare Presentation
PRESENTER: Pavan Patel
PRESENTER (INSTITUTION ONLY): UMDNJ-NJMS
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Background: Fibrolamellar carcinoma is a very uncommon variant of hepatocellular carcinoma, (HCC)
occurring in 0.6%-8.6% of all hepatocellular carcinoma cases. Unlike HCC, it usually occurs in younger individuals in
their 2nd or 3rd decade of life without any underlying liver disease. Usual cases of metastasis include lymph node,
lung, and peritoneum. We report a unique case of fibrolamellar carcinoma with metastasis to the lumbar spine.
Case Report: This a 27-year-old Hispanic male with no significant past medical history, who presented to the ED with
epigastric and lower back pain for one month. Pain was intermittent, non-radiating, and rated as 10/10 in severity. He
admitted to a 10-15 lb weight loss in the preceding few months, with associated loss of appetite. He denied any
nausea, vomiting, fevers, or chills.
An abdominal US showed a heterogeneous echogenic mass in right lobe of the liver. A CT scan of the abdomen and
pelvis revealed an ovoid enhancing right hepatic lesion with extension into the retroperitoneum. It involved the right
hemidiaphragm and lungs, along with extensive lymphadenopathy, left hydronephrosis, and a lytic L4 lesion. Liver
function tests and AFP were within normal limits, and hepatitis panel was negative. A CT-guided liver biopsy was
obtained, which revealed hepatocellular carcinoma, fibrolamellar variant.
Due to extensive disease, surgical resection was not possible, and therefore, chemotherapy was offered. The patient
was started on Sorafenib and initially did well; however, nine days into the treatment, he developed worsening of
symptoms. The patient and family declined further treatment due to poor prognosis, and opted for home hospice care.
Discussion: This is a unique case of not only an uncommon disease in fibrolamellar carcinoma, but also of a rare
presentation with skeletal metastasis. A literature search revealed only one reported case of metastasis to the
vertebra in a girl with fibrolamellar carcinoma. However, to the best of our knowledge, no other cases have been
reported with bone, lung, lymph node, and retroperitoneal metastasis. Unfortunately, these cases of fibrolamellar
carcinoma do not respond to chemotherapy, and prognosis is poor. Patients with unresectable disease have a 5-year
median survival of 0-5%, and median survival of ≤12 months.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Pavan Patel : ACG Non-Member
Arpita Gandhi : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1734351
TITLE: Immune Reconstitution Inflammatory Syndrome after Infection with Epstein-Barr Virus
PRESENTER: Praveen Mettu
PRESENTER (INSTITUTION ONLY): University of Illinois Hospital
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Background: Immune reconstitution inflammatory syndrome (IRIS) can be a potentially severe complication
of HIV-infected patients’ management and care. As the availability of antiretroviral therapy (ART) continues to expand,
the ability to recognize the heterogeneous presentations of IRIS is paramount. Here, we will describe a case where a
patient with a prior episode of Epstein-Barr virus (EBV) hepatitis developed an inflammatory reaction consistent with
IRIS within the hepatic parenchyma.
Case: A 32-year-old female with a prior history of human immunodeficiency virus (HIV) and a recent history of biopsyproven Epstein-Barr virus (EBV)-related hepatitis, presented to the emergency department for evaluation of fevers,
right upper quadrant pain, and jaundice. Labs were significant for a total bilirubin of 8.0 mg/dL, direct bilirubin of 5.1
mg/dL, alkaline phosphatase of 214 U/L, aspartate aminotransferase level of 1869 U/L, alanine aminotransferase level
of 1446 U/L, total protein of 10.3 g/dL, albumin of 2.9 g/dL, and a prothrombin time of 17 seconds. Acute viral hepatitis
serologies were negative; acetaminophen and alcohol levels were unremarkable. Though EBV IgG titers were
positive, EBV IgM titers were negative. Magnetic resonance imaging of the abdomen was significant for mild porta
hepatis and retroperitoneal lymphadenopathy, splenomegaly, and a normal-appearing biliary system without dilation.
A liver biopsy was obtained, which revealed a T-lymphocyte predominant mixed inflammatory process. Tissue in situ
hybridization confirmed the presence of low level EBV. Given her recent re-initiation of ART after a prior EBV hepatitis,
along with histologic findings, we felt the clinical scenario was representative of an immune reconstitution syndrome.
The patient was started on steroids, with rapid improvement of her liver function tests. Since then, she has been
tapered off steroids and her liver function tests remain normal.
Conclusion: Patients with HIV can develop liver injury through a variety of mechanisms, most notably drug toxicity,
infectious agents, and hepatic steatosis. IRIS is a rare, and often challenging, diagnosis. However, it is a highly
treatable cause of abnormal liver enzymes, and, as shown above, identifying the appropriate clinical scenario and
initiation of treatment can result in excellent prognosis.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Praveen Mettu : ACG Non-Member
Miguel Malespin : ACG Non-Member
Maximo Brito : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Somashekar Krishna: [No Comments]|Julia LeBlanc: [No Comments]|Girish Mishra: [No Comments]|Rayburn Rego:
[No Comments]
CONTROL ID: 1734907
TITLE: No Going Back: Noncirrhotic Portal Hypertension in HIV-Infected Patient, 15 Years after Exposure to
Didanosine
PRESENTER: Jose Churrango
PRESENTER (INSTITUTION ONLY): UMDNJ-New Jersey Medical School
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction: The most common cause of portal hypertension is liver cirrhosis. However, portal hypertension
has been described in HIV infected patients without liver disease. Noncirrhotic portal hypertension (NCPH) is
characterized by a non-fibrotic liver accompanied by clinical manifestations, such as bleeding esophageal varices.
Cases of NCPH have been associated with HIV and exposure to anti-retroviral therapy (ART), specifically didanosine,
a nucleoside reverse transcriptase inhibitor. We describe a case of NCPH and resistant esophageal varices in a
patient with remote exposure to didanosine .
Case: A 50-year-old female with morbid obesity, diabetes mellitus type II, and HIV/AIDS for 18 years with a current
CD4 count of 500 and undetectable viral load, was referred for an esophagogastroduodenoscopy (EGD) before
undergoing gastric bypass surgery. The EGD showed three chains of large esophageal varices in the distal
esophagus. Laboratory studies showed a hemoglobin 7.4 gm/dL, MCV 75.2, RDW 17.2, WBC 6.5, platelet count of
204,000, AST 52 U/L, ALT 35 U/L, bilirubin 0.7 mg/dL, alkaline phosphatase 165U/L, albumin of 4.5 gram/dL, and
INR of 1 . A triple phase CT scan was performed, which showed normal liver parenchyma, geographic areas of
peripheral vascular shunting in the liver, splenomegaly, and recannulated umbilical vein with esophageal and
gastrohepatic varices. The hepatic and portal veins were patent. A transjugular biopsy of the liver was performed,
which showed liver tissue with no pathology, and trichome stain was negative for fibrosis. Liver venogram showed
venous pressure gradient of 4 mmHg. Hepatitis serology tests were negative for hepatitis A, B, and C. A medical
history review revealed treatment with didanosine in 1995, which was discontinued after two years. She underwent
banding of esophageal varices multiple times, with recurrence of the varices.
Discussion: The etiology of NCPH is not fully understood, but has been attributed to portal venopathy from alterations
in small vessels and architectural parenchymal changes of the liver. This entity has been associated with thrombosis
of portal venules and endothelial injury by factors directly or indirectly related to HIV infection. In addition,
nucleotide/nucleoside reverse transcriptase inhibitors (NRTIs), specifically didanosine, may have a synergistic effect
on portal venopathy by injuring the vessels’ endothelium through mitochondrial damage. Our case demonstrates that
didanosine-induced portal hypertension can develop many years after discontinuation of the drug. This appears to be
an irreversible process, since repeated banding in our patient did not eradicated the varices.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Jose Churrango : ACG Non-Member
Sami Samiullah : ACG Member
Fatima Samad : ACG Non-Member
Hadi Bhurgri : ACG Non-Member
Zamir Brelvi : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: Minor grammatical errors, but overall very well written.|Selvi Thirumurthi: [No Comments]|Renu
Umashanker: [No Comments]|James Vecchio: [No Comments]
CONTROL ID: 1735689
TITLE: Niacin-Induced Cholestatic Hepatitis in a Cirrhotic Patient
PRESENTER: JayaKrishna Chintanaboina
PRESENTER (INSTITUTION ONLY): Wright Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Although there are several reported cases of niacin-induced hepatotoxicity, niacin-induced cholestatic
hepatitis (CH) is very rarely reported in the medical literature. We report a case of niacin-induced CH in a patient with
liver cirrhosis.
A 61-year-old man with CAD, hyperlipidemia, prostate cancer and status-post prostatectomy was referred for
abnormal liver function tests (LFTs). He had thrombocytopenia, which was incidentally found during the preoperative
work-up of an elective hernia repair. Home medications included omeprazole, aspirin, clopidogrel, metoprolol and
niacin. He was taking niacin-SR 2 gm daily for approximately 6 months. He denied history of alcohol abuse. Physical
examination was remarkable for jaundice, ascites and mild pitting edema of legs. Lab data is shown in the table.
Patient was admitted to the hospital for further work-up of the progressively worsening LFTs. Niacin was held for
severe hepatitis. MRI of the abdomen showed small nodular liver, moderate ascites and a distended gallbladder with
multiple gall stones. HBsAg, Hep C antibody and Hep A IgM antibody were non-reactive. Serological work up for
hemochromatosis (including gene mutation analysis), autoimmune hepatitis and Wilson’s disease were negative.
Tumor markers including serum alpha-feto protein, serum carcinoembryogenic antigen and serum prostate specific
antigen levels were non-significant. Liver biopsy showed moderate-severe chronic active hepatitis, bridging fibrosis
without evidence of malignancy. Liver enzymes gradually trended down with conservative management after stopping
niacin.
Niacin was not initially suspected as the cause of this decompensation due to the primary cholestatic profile. However,
it was later attributed to niacin as he developed CH during treatment with the drug; he improved immediately after
stopping the drug, while other potential causes were ruled out. To our knowledge, there is only one reported case of
niacin-induced CH (Patel SD et al., 1994). Clinicians should be aware of this rare association of niacin with CH;
cirrhotic patients may be more vulnerable.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Alexander Lalos : ACG Member
JayaKrishna Chintanaboina : ACG Member
(No Image Selected)
Laboratory data on hospital admission
Laboratory data
Results
Normal Values
Serum Alkaline
1525 U/L
30-120
232 U/L
7-40
313 U/L
8-42
Serum total bilirubin
9.2 mg/dL
0.4-1.4
Serum direct bilirubin
3.6 mg/dL
0-0.4
Prothrombin time
13.1 sec
11.7-14.7
INR
1.01
<1.1
Platelets
86,000 /uL
142,000-424,000
Serum albumin
1.9 g/dL
3.5-5.0
Phosphatase
Serum alanine
transaminase
Serum aspartate
transaminase
TABLE TITLE: Laboratory data on hospital admission
AVERAGE SCORE: 5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: Based on case presentation, it appears that the diagnosis of liver cirrhosis was also a new one. It is
unclear as to what caused the underlying cirrhosis -- ? secondary to NASH. Acute cholestatic injuury felt to be
secondary to Niacin.|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No Comments]|James Vecchio: [No
Comments]
CONTROL ID: 1735702
TITLE: One Train Can Hide Another: Ascites in a Cirrhotic Patient
PRESENTER: Kawtar Alkhalloufi
PRESENTER (INSTITUTION ONLY): Florida Hospital
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Peritoneal infiltration with myeloma cells has rarely been reported to occur in multiple myeloma. We present
a case of a 53-year-old man with a history of hepatitis C-induced liver cirrhosis complicated by hepatocellular
carcinoma s/p transarterial chemoembolization and history of decompensation of his liver disease in the form of
ascites , hepatic encephalopathy, and variceal bleed s/p banding. The patient presented to the hospital with the
complaint of fatigue, decrease appetite, increase of abdominal girth, and confusion of four weeks' duration. On
physical exam, the patient was found to have temporal wasting, ascites, hepatomegaly, and bilateral lower extremities
edema. The blood work revealed a normocytic anemia with a hemoglobin of 10.0 and hematocrit of 30.8 , mild
thrombocytopemia with platelet count of 137, INR 1.75, total protein of 7.5, albumin of 2.1, globulin level of 5.4, total
bilirubin was 2.8, alkaline phosphatase was 156, ALT of 16 , AST of 49, and a MELD score of 17. The patient
underwent a large-volume paracentesis, with a removal of six liters of yellow hazy fluid, and the analysis was
consistent with spontaneous bacterial peritonitis. The flow cytometry demonstrated an intracytoplasmic lambda
monoclonal plasma cell population, favoring a plasma cell myeloma. The SPEP showed hypergammaglobulenemia
with a monoclonal spike measuring 0.56 g/dl, and the immunofixation demonstrated an igM Lambda. The peripheral
smear showed normochromic normocytic anemia with slight rouleau. The bone marrow aspirate revealed
plasmocytosis consistent with a plasma cell neoplasm. The plasma cells comprised approximately 30-40% of the bone
marrow cellularity, and were monotypic for lambda light chain. Cytoplasmic immunoglobulin FISH for multiple
myeloma was performed, and was positive for four copies of 1q21, an extra copy of CCND1, and an extra copy of IgH,
which is consistent with high-risk disease and an adverse prognosis.
The bone scan was negative of any osteolytic lesions. The patient was diagnosed with multiple myeloma; however,
during the course of the hospitalization, the patient developed septic chock with candidemia and acute hypoxic
respiratory and renal failure, for which he was intubated started on pressors, large spectrum antibiotics, and fungal
therapy. Unfortunately, the patient’s condition deteriorated, and he expired on day seven of the hospital stay.
In conclusion: In our opinion, the ascitic fluid analysis, including the pathology, should be performed in all patients
presenting with ascites, even in the setting of a known, underlying cause of ascites.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Kawtar Alkhalloufi : ACG Member
Juan Blum Guzman : ACG Member
Edula Raja : ACG Non-Member
Zahid Vahora : ACG Non-Member
Hicham Khallafi : ACG Non-Member
Kamran Qureshi : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: Not sure what prompted flow cytometry of the ascitic fluid in the first place. Key element missing in
the abstract.|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No Comments]|James Vecchio: [No Comments]
CONTROL ID: 1735849
TITLE: Nonischemic Cardiomyopathy Secondary to Pegylated Interferon in a Patient with Chronic Hepatitis C
PRESENTER: Shail Sheth
PRESENTER (INSTITUTION ONLY): Saint Michael's medical center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Reversible cardiomyopathy is a side effect of interferon treatment, typically described as being associated
with high-dose standard interferon. Pegylated INF has a polyethylene glycol molecule attached to the protein, which
results in a reduction in its rate of absorption, renal clearance, and immunogenicity following subcutaneous injection.
We present a rare case of PEG interferon-induced dilated cardiomyopathy. A 65-year-old female with hepatitis C
(HCV), mononeuritis multiplex, mixed cryoglobulinemia, and hypertension presented with complaints of shortness of
breath with minimal exertion, which was gradually worsening. She denied any chest pain, palpitations, fever, chills,
blood loss, weight loss, or history of smoking. She was started on treatment for HCV in June of 2012, with telapravir,
PEG interferon, and ribavirin. Her viral load was detectable at week four, and undetectable at weeks 12 and 24. Her
renal function was normal at the start of treatment. During the therapy, her renal function started to deteriorate. Doses
of ribavirin and interferon were reduced secondary to her anemia and neutropenia, respectively. Despite dose
reduction, treatment was stopped at week 33 due to treatment intolerance. Prior to treatment, the patient had a
cardiac catheterization, which showed an ejection fraction (EF) of 50% and non-obstructive coronary artery disease.
An echocardiogram done in following treatment showed an EF of 30-35%, with moderate mitral regurgitation (MR) and
global left ventricular hypokinesia, stage three diastolic dysfunction, left ventricular dilatation, moderate left atrial
dilatation, trace tricuspid regurgitation, and a pulmonary artery pressure of 40 mmHg. A transesophageal
echocardiogram (TEE) confirmed the global hypokinesia, and the EF had decreased to 15-20%, with moderate MR.
Repeat cardiac catheterization showed global hypokinesia, patent coronary arteries, and an EF of 25-30%. The right
ventricular systolic pressure was 41 mmHg. Cryoglobulins were absent, and the rheumatoid factor had decreased to
45 from 200 prior to treatment. An autoimmune work-up was negative. The patient denied any flu-like illness during
treatment. A myocardial biopsy was not performed to confirm the diagnosis; however, after ruling out other causes of
cardiomyopathy, we attributed the cardiomyopathy to interferon therapy. We believe that the deterioration in renal
function may have caused elevated concentrations of interferon, resulting in cardiotoxicity. The sudden worsening of
the cardiomyopathy and its chronology in relation to the use of pegylated interferon and deteriorating renal function
further support our impression.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Shail Sheth : ACG Non-Member
Nhat Nguyen : ACG Non-Member
Joseph DePasquale : ACG Non-Member
Gautamy Chitiki-Dhadham : ACG Non-Member
Robert Spira : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: grammatical errors. Loose ends - degree of renal impairment never elaborated on (? Cr) nor was the
cause of renal impairment given|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No Comments]|James
Vecchio: [No Comments]
CONTROL ID: 1735929
TITLE: Hepatitis and Pancreatitis Associated with the Use of Trimetropim Sulfamethoxazole: A case Report
PRESENTER: Laura Hernandez
PRESENTER (INSTITUTION ONLY): Northshore University
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Purpose/Introduction: Trimetropim sulfamethoxazole (TMP-SMX) is a widely prescribed antibiotic. Both
hepatitis and pancreatitis are uncommon side effects, and reports in non-immunosuppressed patients are rare. To our
knowledge, there are only two previous case reports of concomitant hepatitis and pancreatitis occurring in an
inmunocompetent patient.
Case Presentation: A 65-year-old male with previous history of coronary artery disease, hypertension and
dyslipidemia presented to the emergency room with abdominal pain, jaundice and a skin rash. The patient had been
started on TMP-SMX for otitis media two weeks before arriving to the emergency department. During this period of
time, the patient presented with nausea, vomiting, weight loss and fever. On physical examination, he was found to be
jaundice, and a generalized non-pruritic macular rash was noticed. There was no history of alcohol use.
On admission, liver function test and pancreatic markers were elevated. ALT peaked to 510, AST to 445 U/L, total and
direct bilirubin to 19 and 8.9 mg/dL respectively, lipase to 578 U/L and amylase 102 U/L, albumin was decreased and
coagulation studies were normal, and remained normal during and after hospitalization. Other causes of pancreatitis
were rule out. Triglycerides were within normal limits and calcium and SPEP were normal. Acute viral hepatitis, CMV
and EBV serology were negative, and titers of autoimmune markers were normal. Abdominal CT did not show hepatic
or pancreatic abnormalities, and the abdominal ultrasound did not show gallstones or dilation of the intrahepatic ducts.
Upper endoscopy showed esophagitis and gastritis.
Pancreatitis and hepatitis were managed with fluid resuscitation and supportive care. The patient improved clinically, a
decrease in lipase and aminotransferase was noted during hospitalization and a gradual decrease of bilirubin occurred
after hospitalization.
Discussion: Clinical observation is an important tool to identify adverse effects from medications. In this particular
case, we have a Naranjo score of six (probable drug reaction). The mechanism of idiosyncratic adverse effects to
TMP-SMX is not clearly understood, but inmuno-allergic mechanisms have been proposed. This case underlines the
importance of considering commonly used medications as the causative event of severe medical conditions.
Methods: NA
Results: NA
Conclusion: NA
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Industry
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Jonathan Williams : ACG Member
Laura Hernandez : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: Very well written.|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No Comments]|James
Vecchio: [No Comments]
CONTROL ID: 1736269
TITLE: Telaprevir Induced Pancreatitis Complicating Hepatitis C Treatment
PRESENTER: Vu Nguyen
PRESENTER (INSTITUTION ONLY): Wake Forest Baptist Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: We describe a case of telaprevir-induced pancreatitis and the subsequent outcome of completed course of
therapy for hepatitis C.
Case: A 55-year-old female with Genotype 1 hepatitis C infection had been a partial responder to prior therapy with
ribavirin and peginterferon alfa 2a. This course of therapy was discontinued after 11 weeks when she developed
symptomatic hyperthyroidism. Three years later, treatment was reinitiated with ribavirin, peginterferon alfa 2a and
telaprevir. In her 7th week of therapy, she presented with acute pancreatitis requiring hospitalization. Her labs on
admission showed amylase of 5,946 u/L, lipase > 2,000 u/L and normal LFTs. Abdominal CT revealed fluid adjacent
to the pancreatic head, consistent with acute pancreatitis. Ultrasound at the time and subsequently showed “possible
small gallbladder stones versus sludge.” MR cholangiography was negative for filling defects or ductal dilation. Serum
triglycerides and IgG4 level were normal. She denied alcohol use and had no family or personal history of pancreatitis.
Other medications on admission were not known to cause pancreatitis. She was managed conservatively and
improved. Her triple therapy regimen was continued during the five days of hospitalization. Amylase, lipase, AST, ALT
were 127, 90, 48 and 32 u/L respectively on discharge. In close follow-up five days later, she remained asymptomatic,
although her amylase and lipase had risen to 173 and 333 u/L. In the following week, she developed severe
abdominal pain and was readmitted. Admission labs: amylase 3,714, lipase > 2,000, AST 85, ALT 51 u/L. All of her
hepatitis C medications were held. She quickly improved with conservative management and was discharged 4 days
later. LFTs continued to trend down and lipase had normalized on the day of discharge. She had received nine weeks
of telaprevir. Six days after discharge, she was clinically stable, and ribavirin and peginterferon alfa 2a were restarted
at her prior dose. She had no further episodes of recurrent pancreatitis. Her amylase and lipase were normal on
repeat labs, and she completed 48 weeks of therapy. At three and six months post completion of therapy, HCV RNA
level was undetectable.
Discussion: To date, there has been only one other report of telaprevir-induced pancreatitis. Our case is the first to
describe the natural course of this idiosyncratic reaction and its effect on HCV therapy. Although there have been
reports of ribavirin and peginterferon causing acute pancreatitis, in this patient with telaprevir-induced pancreatitis,
ribavirin and peginterferon alpha 2a were continued without any further complication of recurrent pancreatitis.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Vu Nguyen : ACG Non-Member
Daniel Murphy : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: There is no detail about how hyperthyroidism was treated.
She was retreated with the same agents that caused hyperthyroidism 3 years ago requiring discontinuation of
treatment.
The authors never speculate as to why pancreatic enzymes went down after the first episode of pancreatitis even
though the teleprevir was continued. Does not make sense that the enzymes would have gone down if telaprevir is
felt to be the cause of the 2 episodes of pancreatitis.|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No
Comments]|James Vecchio: [No Comments]
CONTROL ID: 1736706
TITLE: Seronegative Autoimmune Hepatitis and Concomitant Membranous Glomerulonephritis
PRESENTER: Siddharth Sura
PRESENTER (INSTITUTION ONLY): Emory University School of Medicine, Division of Digestive Diseases
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Background: Autoimmune hepatitis (AIH) is characterized by chronic inflammation due to immunologic
injury, generally associated with circulating autoantibodies and hypergammaglobulinemia. Membranous
glomerulonephritis (MGN) is a rare, extrahepatic manifestation of AIH. We present the case of a patient diagnosed
concomitantly with seronegative AIH and MGN.
Case: A 28 year-old previously healthy male presented with flu-like symptoms and abdominal pain of two weeks'
duration. He had diffuse anasarca, abdominal distention, and marked lower extremity edema. He was hospitalized for
further evaluation after laboratory data revealed nephrotic-range proteinuria (16.6 g/day on 24 hour urine) and marked
hepatocellular injury (ALT 1346 U/L and AST 1661 U/L). Notably, his mental status remained intact, and he did not
have evidence of coagulopathy. Extensive serologic work-up was unrevealing, including for viral hepatitis,
autoimmune serologies, metabolic disorders, and drug-induced liver injury. Imaging showed ascites and perigastric
varices. Liver biopsy revealed severe interface hepatitis comprising predominantly of plasma cells and >40% hepatic
necrosis (Figure 1). Renal biopsy showed stage I MGN with minimal interstitial fibrosis, and no tubular atrophy.
Corticosteroid therapy was initiated with rapid improvement of symptoms and marked decrease in transaminases.
Liver biopsy, after two months of treatment, showed complete resolution of interface hepatitis and necrosis.
Unfortunately, his proteinuria continued to persist, and mycophenolate was initiated for concomitant immunomodulator
therapy.
Discussion: The relationship between MGN and AIH is unclear. Although typically idiopathic, MGN can be associated
with autoimmune conditions. The causative agent in this particular case could be the deposition of immune
complexes due to active AIH, which can disrupt the basement membrane in renal glomeruli. Particularly interesting is
that although management of secondary MGN is to treat the underlying process, our patient’s proteinuria persisted,
despite near resolution of hepatocellular inflammation.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Ravi Vora : ACG Non-Member
Siddharth Sura : ACG Member
Kun Jiang : ACG Non-Member
Anjana Pillai : ACG Member
Figure 1
IMAGE CAPTION: Figure 1
(no table selected)
AVERAGE SCORE: 4.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: Not sure that this is truly a novel topic/concept.|Selvi Thirumurthi: [No Comments]|Renu
Umashanker: [No Comments]|James Vecchio: [No Comments]
CONTROL ID: 1737329
TITLE: Hepatic Hydrothorax: Dos and Don'ts
PRESENTER: Parag Brahmbhatt
PRESENTER (INSTITUTION ONLY): East Tennessee State University
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction: Hepatic hydrothorax is defined as a transudative pleural effusion, usually greater than 500 mL,
in patients with portal hypertension without any other underlying primary cardiopulmonary cause.
Case report: A 54-year-old patient with history of cirrhosis secondary to NASH came to the hospital secondary to
worsening lethargy and fatigue. The patient also noticed a 10-lb weight gain, mild shortness of breath on excretion,
and abdominal distention without any fever. Blood pressure was 100/50 mmhg and HR of 92/min. Physical
examination revealed mild bibasilar crackles and distended abdomen with periumbilical tenderness. The patient
refused paracentesis, and was started on furosemide and spironolactone with improvement in symptoms. On hospital
day three, the patient started complaining of worsening abdominal pain, and then became confused. Lactate level was
elevated at 4.1 mmol/L, along with ammonia level of 257 mcmol/L. CT scan of the abdomen showed possible
ischemic colitis. The patient underwent emergent exploratory laparotomy, which did not show any necrotic bowel. The
patient was intubated and transferred to ICU, and was weaned off after 4four days, and was then discharged to rehab
facility. While in the rehab, the patient started feeling more SOB, and CXR showed large right sided plural effusion.
Thoracentesis was performed with removal of 4300 cc of dark yellow fluid. Post-procedure CXR showed improvement,
but CXR next day again showed worsening right-sided plural effusion. A chest tube was placed, which resulted in the
worsening of patient’s condition with leukocytosis. He was transferred to higher center, where the chest tube was
removed, and was then treated with appropriate antibiotics and diuretics.
Discussion: The most likely cause of pleural effusions in patients with cirrhosis is the passage of a large amount of
ascites from the peritoneal to the pleural cavity, through diaphragmatic defects. Plural effusion is unilateral in the
majority of cases, with right-sided predominance. Initial management consists of sodium restriction and diuretics.
Other treatment options include thoracentesis, TIPS, and liver transplant. Thoracentesis is indicated for symptomatic
relief, as well as for patients with refractory hepato-hydrothorax. Liver transplant is the only definite treatment.
Dos: Suspect hepatic hydrothorax in patients with liver cirrhosis and unilateral plural effusion. Perform large volume
paracentesis prior to thoracentesis. Consider alternative treatment when a thoracentesis is required more than once
every two to three weeks in patients on maximal sodium restriction and optimal diuretics.
Don’ts : Do not put chest tube unless frank pus is noted on thoracentesis. Do not remove more than two L of fluid
during thoracentesis.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Parag Brahmbhatt : ACG Member
Mehul Panchal : ACG Non-Member
Fagun Modi : ACG Non-Member
Atif Saleem : ACG Member
Mark Young : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: [No Comments]|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No Comments]|James
Vecchio: [No Comments]
CONTROL ID: 1737911
TITLE: Expecting the Unexpected: Black Cohosh-Induced Hepatotoxicity Leading to Early Cirrhosis
PRESENTER: Khadija Chaudrey
PRESENTER (INSTITUTION ONLY): University of Oklahoma Health Sciences Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Herbal supplements are commonly used by patients for various problems. It is a well-known fact that most
patients do not tell their physicians regarding use of herbal supplements unless specifically asked. As a result,
sometimes important points from drug side effects are missed in history taking. In this context, we present a rare case
of Black Cohosh-induced hepatotoxicity leading to early cirrhosis.
Case Description: A 44-year-old female with no PMH presented with complaints of painless jaundice for one month.
She went to her PCP, where initial work-up revealed that she had elevated LFTs. She was noted to have normal LFTs
on her prior lab works. Work-up for viral and autoimmune hepatitis was negative. She was given a trial of steroids on
outpatient basis without much improvement. She was referred to inpatient evaluation because of gradual progression
of her symptoms. She denied history of alcohol intake, IV drug use, unprotected sex, recent travel outside the U.S.,
NSAID ingestion or blood transfusions. She reported no abdominal pain, fever, chills, nausea vomiting or diarrhea.
She did report generalized itching, arthralgia and fatigue. She interestingly reported that she started taking Black
Cohosh for alleviation of her menstrual symptoms about one month back. Her exam was remarkable for marked
scleral icterus and jaundiced skin. On admission, her LFT showed TBil =20, AST=420, ALT=215, AlkPhos=201,
Platelets=135, INR 1.2 and Albumin=2.4. Ultrasound abdomen showed nodular contour of liver consistent with
cirrhosis. Further work-up ruled out Wilson’s disease, Hemochromatosis, AMA negative PBC and autoimmune
hepatitis. Liver biopsy was performed, which showed histologic pattern consistent with cholestasis, hepatocellular
injury and early cirrhosis. Given patient’s history of Black Cohosh use and the timing of her abnormal liver chemistries,
it was clinically evident the culprit agent was Black Cohosh. Her symptoms improved, and her LFT’s normalized after
she stopped taking Black Cohosh.
Discussion: Black Cohosh, also named as Cimicifuga racemosa, is among commonly used herbal supplements in the
United States for menstrual symptoms. There are few case reports available in literature that attribute Black Cohosh to
liver injury. In most instances, the liver injury ranges from jaundice, mild transaminasemia to rare cases of fulminant
hepatic failure. Our case is unique, since it represents development of accelerated cirrhosis in our patient for a
relatively short period of time. This case is to bring awareness amongst clinicians about this potentially unexpected
outcome in the backdrop of much-expected drug induced hepatitis.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Khadija Chaudrey : ACG Non-Member
Muhammad Khan : ACG Non-Member
Javid Fazili : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: not very well organized.
Also it is a bit of a jump that the black cohosh caused cirrhosis to develop within 1 month. We do not know whether or
not she had pre-existing disease.|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No Comments]|James
Vecchio: [No Comments]
CONTROL ID: 1737925
TITLE: Spontaneous Tumor Rupture as the Initial Manifestation of Primary Hepatic Leiomyosarcoma (LMS)
PRESENTER: Bhavtosh Dedania
PRESENTER (INSTITUTION ONLY): University of Connecticut Health Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 42-year-old male with no significant past medical history presented to the emergency room with severe
sudden onset right upper quadrant abdominal pain and nausea, developed over hours. Physical examination revealed
tender hepatomegaly without any signs of peritonitis. Contrast-enhanced computed tomographic scan of abdomen
showed a 13.7 x 11.4 x 11.8 cm, well circumscribed, heterogeneous dense mass in the right lobe of the liver, with the
evidence of sub-capsular and free intra-peritoneal hemorrhage. Gadolinium-enhanced magnetic resonance imaging
showed a centrally increased T1 signal consistent with internal hemorrhage, and a T2 hypo-intense rim compatible
with a capsule or pseudo-capsule. No lymph node involvement or vascular obstruction was noted. Diagnostic
laboratory data was fairly benign, including alpha-fetoprotein levels. He underwent segment V hepatectomy with
adhesiolysis and evacuation of hematoma. Grossly, the specimen revealed a firm, grey-white mass measuring 20 x 11
x 10 cm with areas of necrosis and hemorrhage. Microscopy revealed areas of fascicular growth in a highly
pleomorphic neoplasm with high mitotic count and abundant necrosis with storiform and myxoid areas, suggestive of
LMS. The tumor cells were positive for desmin stain, but negative for smooth muscle actin, S-100, DOG-1, CD 117,
and epithelial membrane antigen. He had an uneventful post-op recovery, and seven months after the surgery, he is
doing well, with no recurrence.
Primary hepatic LMS is usually asymptomatic, and can attain a fairly large size before symptom development. It is
found more often in patients with Epstein-Barr virus infections, lymphoma, or post-renal transplant patients. Unlike
other hepatocellular cancers (HCC), imaging and serological markers aren’t helpful in diagnosis, and the cornerstone
for diagnosis is usually histopathology. Surgical resection of tumor with R0 tumor-free margin resection offers the best
outcome. The roles of chemotherapy, radiotherapy, and liver transplant in these tumors are not clearly defined yet.
Primary hepatic LMS is a rare tumor comprising < 2% of all HCC, which should be included in the differential
diagnosis of a hepatic mass in the absence of imaging features or serological markers suggestive of HCC. Surgical
resection is the best available treatment for now.
Methods: NA
Results: NA
Conclusion: NA
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: Yes
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Bhavtosh Dedania : ACG Non-Member
Shounak Majumder : ACG Member
Houman Rezaizadeh : ACG Member
Michael Einstein : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: poor syntax in first sentence|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No
Comments]|James Vecchio: [No Comments]
CONTROL ID: 1739844
TITLE: Hepatotoxicty from Combined Use of Acetaminophen and Phenobarbital
PRESENTER: Jonathan Umbel
PRESENTER (INSTITUTION ONLY): University Hospital/Case Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 48-year-old Caucasian male with known chronic hepatitis C infection presented to the emergency
department following an intentional phenobarbital overdose. He had been maintained on phenobarbital for many
years, due to an underlying seizure disorder. There was no other evidence of illicit, prescribed or over-the-counter
medication use. On presentation, he was unresponsive, hypotensive and bradycardic. The patient was intubated for
airway protection and admitted to the intensive care unit. Toxicology screens, acetaminophen levels and aspirin levels
were negative except for significantly elevated phenobarbital levels. On admission, his liver transaminases were mildly
elevated (but stable and consistent with his prior known HCV). He was treated with supportive care and eventually
extubated. Several days later in the hospitalization, he developed right-sided abdominal pain. Evaluation was
consistent with severe colitis, which eventually required an uneventful right hemicolectomy. The LFTs remained
stable. Post-operatively, he was started back on phenobarbital. His pain medication regimen was intravenous
acetaminophen 1,000 mg every six hours as needed. Three days later, the patient was noted to be jaundiced. Liver
function tests revealed AST 1690, ALT 1851, alkaline phosphatase 536 and bilirubin 4.7. Ultrasound with Doppler
studies demonstrated gallbladder sludge, but no acute liver or biliary pathology. Workup for other causes of acute liver
disease including hepatitis A, hepatitis B, autoimmune hepatitis, Wilson disease and alpha-1-antitrypsin deficiency
were negative. He was felt to likely have acetaminophen toxicity as the cause of the elevated LFT’s. Acetaminophen
was discontinued and the transaminases rapidly returned to baseline. This case illustrates several important points
regarding acetaminophen hepatotoxicity. First, acetaminophen is metabolized by the cytochrome P450 system into its
toxic metabolite, N-acetyl-p-benzoquinone imine. Second, potent inducers of CYP2E1, such as phenobarbital, can
significantly increase the levels of the toxic metabolite causing increased risk for acetaminophen hepatotoxicity. Third,
this toxicity can even occur within the expected therapeutic levels of acetaminophen. In conclusion, acetaminophen,
especially in the intravenous form, should be used with caution in patients taking medications that affect its
metabolism due to an increased risk of hepatotoxicity.
Methods: NA
Results: NA
Conclusion: NA
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Jonathan Umbel : ACG Non-Member
Aditi Saxena : ACG Member
Pierre Gholam : ACG Member
Anthony Post : ACG Member
Badar Muneer : ACG Non-Member
Stanley Cohen : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: Nothing new here. Written well but really there are no new concepts here.|Selvi Thirumurthi: [No
Comments]|Renu Umashanker: [No Comments]|James Vecchio: [No Comments]
CONTROL ID: 1740818
TITLE: An Unusual Complication of Splenic Artery Coil Embolization
PRESENTER: Dina Ahmad
PRESENTER (INSTITUTION ONLY): University of Missouri - Columbia
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Splenic coil embolization is now considered one of the main therapies for hypersplenism in cirrhotic patients.
Previous interventions, including splenectomy and splenic artery ligation, were associated with overwhelming
complications, including sepsis, splenic abscess formation, and splenic rupture. We present an interesting case of a
cirrhotic patient who underwent splenic artery coil embolization and developed serious, life-threatening complications.
Case: A 50-year-old male with decompensated liver cirrhosis secondary to chronic hepatitis C underwent splenic
artery coil embolization one week prior to his hospital presentation. He presented to the emergency department
complaining of left-sided abdominal pain that radiated to the left shoulder, nausea, and loss of appetite for four days'
duration. He denied fever, chills, vomiting, melena, or diarrhea. Vital signs were stable, except for tachycardia 105
bpm. Physical examination showed decreased air entry at bilateral lung fields and lower extremity edema. Abdominal
examination revealed splenomegaly, hepatomegaly, and ascites with tenderness in left upper and lower quadrants.
Abnormal labs included WBC 17,400/mm3, platelets 100,000/mm3, creatinine 1.26 mg/dL, potassium 5.5 mmol/L,
AST 48 unit/L, INR 2.4, total bilirubin 3.6 mg/dL, and lactic acid 4.6 mmol/L. Ascitic fluid analysis revealed neutrophil
count > 250 cells/µL. Abdominal computed tomography scan showed splenomegaly with evidence of splenic coils, two
moderate-sized splenic infarcts, cirrhosis, portal hypertension, gastric and esophageal varices, ascites, and bilateral
pleural effusions. The patient was started on broad-spectrum antibiotics initially, until blood and ascitic fluid cultures
revealed methicillin-resistant Staphylococcus aureus. His hospital stay was complicated with multi-organ failure due to
sepsis, which required ICU admission and intubation. His complicated course was believed to be due to splenic artery
coil placement, causing secondary peritonitis and sepsis.
Conclusion: Indications for splenic embolization are numerous, and include hypersplenism, splenic trauma, and
hematologic disorders. Major complications arising from splenic artery coil embolization are very rare. This case
represents a rare and life-threatening complication after undergoing splenic artery coil embolization.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Dina Ahmad : ACG Non-Member
Alisha Hinds : ACG Non-Member
Kristi Lopez : ACG Member
Murtaza Arif : ACG Member
Michelle Matteson : ACG Member
Matthew Bechtold : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: [No Comments]|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No Comments]|James
Vecchio: [No Comments]
CONTROL ID: 1741127
TITLE: Between a Gallstone and a Hard Place: Type II Gallbladder Perforation in a Cirrhotic Patient
PRESENTER: Brian Hanson
PRESENTER (INSTITUTION ONLY): University of Minnesota
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 62-year-old man with ESLD secondary to sarcoidosis presented with abdominal pain. Laboratory data
revealed: total bilirubin 5.4 mg/dL, creatinine 1.1 mg/dL, INR 1.47, WBC 9,500/cmm. Model for end-stage liver disease
(MELD) score was 18. CT abdomen displayed a stone containing intrahepatic abscess. Antibiotics were initiated.
Percutaneous drainage was performed, yielding purulent fluid. Culture grew klebsiella oxytoca. The patient became
septic and developed renal failure, with rise in MELD score to 30. Surgical abscess resection with cholecystectomy
was deemed too high-risk. Emergent liver transplantation was considered. While wait listed, the patient improved with
supportive therapy. The abscess cavity closed, and the drain was removed. Extrapolating data from retained renal
stones, the gallstone was believed to be a nidus for continued infection. The patient continues on suppressive
antibiotics while awaiting liver transplant.
Gallbladder perforation is a rare complication of cholecytitis. A single case of gallbladder perforation and abdominal
wall abscess in a patient with ESLD has been reported. Percutaneous cholecystostomy was unsuccessful, and partial
open cholecystectomy was performed. Liver transplantation was attempted, but the patient died from surgical
complications. Ours is the first case report of gallbladder perforation with a retained intrahepatic gallstone and
associated abscess in a patient with ESLD. While case reports exist of retained intrahepatic stone after gallbladder
rupture, these occurred in patients without ESLD or contraindications to surgery. These patients were treated with
surgical stone abstraction and cholecystectomy. Elective surgery in patients with Child-Turcotte-Pugh C cirrhosis is
contraindicated. In our case, the retained gallstone remained a source for infection, and without definitive therapy,
there remained potential for clinical deterioration. Our patient improved with conservative therapy, and emergent
transplant was not necessary. Direct evidence for suppressive antibiotic therapy does not exist, but given the uneven,
porous surface of gallstones and the experience with retained renal stones, it is reasonable to continue antibiotics in
such cases.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Brian Hanson : ACG Non-Member
James Roat : ACG Non-Member
Christine Pocha : ACG Member
Arrow indicates gallstone within an intrahepatic abscess.
IMAGE CAPTION: Arrow indicates gallstone within an intrahepatic abscess.
(no table selected)
AVERAGE SCORE: 5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: th description of the case never mentions the gallbladder perforation
CT findings are confusing.|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No Comments]|James Vecchio: [No
Comments]
CONTROL ID: 1741333
TITLE: Salvage Treatment with Boceprevir-based Triple Therapy After Failed Treatment of Acute Hepatitis C with
Dual Therapy
PRESENTER: Nabil Mansour
PRESENTER (INSTITUTION ONLY): University of Kansas School of Medicine-Wichita
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Acute hepatitis C virus (HCV) infection is usually defined by the presence of signs or symptoms of hepatitis
within six months of presumed HCV exposure. While the majority of patients with acute HCV infection are
asymptomatic, some do present with symptoms. Treatment of acute HCV infection with interferon is recommended in
patients who do not spontaneously clear the virus within 12 weeks of diagnosis, and the vast majority of patients
(>80%) who are treated will have a sustained virologic response (SVR) with interferon alone. Recommendations are
lacking, however, for patients who do not respond well to standard treatment of acute hepatitis C, and at this time, the
use of protease inhibitors in the treatment of acute HCV infection is not widely advocated. We present a case of acute
HCV infection that was treated with boceprevir-based triple therapy after failure of treatment with combined pegylated
interferon and ribavarin.
A 24-year-old female was admitted to the hospital with abdominal pain, vomiting and jaundice. Her transaminases
were elevated, with ALT 673 and AST 971. Work-up revealed positive HCV antibodies, with HCV RNA viral load of 3.1
million copies and genotype 1b. The patient had been hospitalized one month prior, and HCV antibodies were
negative at the time, indicating a recent infection consistent with acute hepatitis C. Follow-up eight weeks after
diagnosis revealed HCV RNA of 5760 copies, with hopes that the patient would spontaneously clear the virus by 12
weeks. However, the HCV RNA viral load increased to 165,160 copies at 12 weeks, and the patient was started on
treatment with combined pegylated interferon and ribavarin. The patient failed to respond, however, and after 12
weeks of dual therapy, her HCV RNA had actually increased to 327,000 copies. At this point, given the evident lack of
response to combined pegylated interferon and ribavirin, it was decided to add a protease inhibitor, and boceprevir
was added without an interruption in therapy, with plans to treat with triple therapy for an additional 44 weeks. Four
weeks after the addition of boceprevir, the patient's HCV RNA viral load was undetectable and has remained
undetectable at end of treatment (pending SVR).
As this case illustrates, immediate initiation of protease inhibitor-based triple therapy may be a reasonable treatment
option in patients with acute genotype 1 HCV infection who do not respond to standard therapy. Studies are needed to
better determine the efficacy and optimal duration of treatment in this patient population.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Nabil Mansour : ACG Non-Member
Mustapha El-Halabi : ACG Non-Member
William Salyers : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 2.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: [No Comments]|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No Comments]|James
Vecchio: [No Comments]
CONTROL ID: 1741591
TITLE: Eosinophilic Cholangitis as an Unusual Presentation of Hypereosinophilic Syndrome
PRESENTER: Mariajose Rojas De Leon
PRESENTER (INSTITUTION ONLY): John H. Stroger Jr. Hospital of Cook County, Department of Gastroenterology
and Hepatology
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Eosinophilic Cholangitis is a rare disorder of unknown etiology, characterized by eosinophilic infiltration of
the biliary tract.
Case: An 18-year-old male with no significant past medical history presented with a five-day history of left upper
quadrant pain, fever, nausea, and vomiting. He denied recent travel or history of allergies or atopy. Physical exam was
unremarkable, except for LUQ tenderness on palpation. Investigations showed elevated liver function tests (LFT): total
bilirubin 1.6mg/dL, alkaline phosphatase 123, GGT 153, AST 63, and ALT 164. WBC count was 18k/uL with 23%
eosinophils (count 4.3k/uL, normal range 0-0.4). CT abdomen showed ill-defined hepatic hypodensities with mild
surrounding enhancement in the lateral segment of the left lobe and the posterior segment of the right lobe. Hepatitis
virus panel, ANA, AMA, and ASMA were negative. Blood, urine, and stool cultures were negative, and an extensive
infection evaluation for Histoplasma, Toxocara, Trichinella, Strongyloides, Schistosoma and Filaria was also negative.
A liver biopsy showed areas of nonzonal necrosis associated with eosinophilic cholangitis. No viral inclusions,
granulomas, or parasites were seen, and special stains were negative for AFB, fungus, and bacteria. Given the
persistent eosinophilia, a bone marrow aspirate showed marked eosinophilia (42%) without abnormal leucocytes or
cell populations on cytometry. A final diagnosis of idiopathic hypereosinophilic syndrome (HES) with liver involvement
was given. He was treated with prednisone and showed clinical, biochemical, and radiographic improvement.
Discussion: Eosinophilic cholangitis (EC) is part of a spectrum known as eosinophilic cholangiopathy, which can affect
the bile ducts and gallbladder, the gallbladder only (eosinophilic cholecystitis), and, less commonly, the bile ducts (EC)
in isolation. Patients may present with normal or elevated bilirrubin, abnormal LFTs, biliary strictures, and obstructive
jaundice that can mimic disorders such as PBC, PSC, and malignancy. It can present with or without peripheral
eosinophilia, and, rarely, as a manifestation of HES. Diagnosis can be challenging, as there are no specific radiologic
findings. The course of EC is benign and self-limited, with varying degrees of severity, but if untreated and related to
HES, liver fibrosis and organ failure can occur, requiring liver transplant. Most case reports of EC responded favorably
to oral steroids, and those with eosinophilic cholecystitis often undergo cholecystectomy, as presentation can mimic
acalculous cholecystitis. In this case, the response to steroid therapy and a six-year follow up without relapse or
identification of infectious pathogens is consistent with an idiopathic etiology.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Mariajose Rojas De Leon : ACG Member
Melchor Demetria : ACG Member
Bashar Attar : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: [No Comments]|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No Comments]|James
Vecchio: [No Comments]
CONTROL ID: 1741598
TITLE: Fatty Liver is Not Always Fat in the Liver
PRESENTER: Srikrishna Patnana
PRESENTER (INSTITUTION ONLY): University of Mississippi
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 42-year-old Caucasian man with a history of poorly-controlled insulin-dependent diabetes mellitus since
the age of two years was admitted with right upper quadrant pain, nausea, vomiting, and abdominal swelling. He was
found to have an AST of 1190, ALT of 700, ALP of 1465, and a TBili of 1. Comprehensive lab work up was positive for
hepatitis C, amphetamine, and marijuana use, along with an HbA1c of 9.7. Abdominal imaging showed fatty
hepatomegaly. Liver biopsy showed swollen, pale hepatocytes with glycogen accumulation, consistent with glycogenic
hepatopathy (GH). He has had mild intermittent elevated LFTs since 2005, when he had a working insulin pump with
decent control of his diabetes. The insulin pump stopped working one month prior to the current presentation, when he
developed diabetic ketoacidosis.
The term GH was coined by Torbenson et al. in 2006. GH develops in the setting of high glucose and high insulin
levels, which is common in poorly-controlled insulin-dependent diabetics. When blood glucose levels are extremely
high, glucose enters hepatocytes through an insulin-independent mechanism. Excess insulin given for correction of
this hyperglycemia promotes glycogenesis, leading to glycogen deposition in hepatocytes. This condition is
manifested by abdominal pain, hepatomegaly, and elevated LFTs up to 10 times the upper limit of normal. It cannot be
differentiated from the more common non-alcoholic fatty liver disease, clinically or radiologically, as the pattern of LFT
abnormalities are similar, and imaging shows “fatty liver” in both diseases. This is the reason why it is underrecognized. Liver biopsy shows swelling of hepatocytes with glycogen deposition (PAS positive and cleared by
diastase) with no inflammation or hepatocyte necrosis. This is a self-limited condition that improves with better
glycemic control.
Methods: N/A
Results: N/A
Conclusion: Glycogenic hepatopathy in the setting of uncontrolled hyperglycemia need to be considered in the
differential diagnosis of patients who present with elevated liver function tests and steatosis in the liver imaging
studies
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Srikrishna Patnana : ACG Non-Member
Srinivasa Chekuri : ACG Non-Member
Brian Borg : ACG Member
H & E staining of liver biopsy showing accumulation of glycogen in hepatocytes
IMAGE CAPTION: H & E staining of liver biopsy showing accumulation of glycogen in hepatocytes
(no table selected)
AVERAGE SCORE: 4
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: [No Comments]|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No Comments]|James
Vecchio: [No Comments]
CONTROL ID: 1741633
TITLE: Obstructive Jaundice in Hodgkin’s Lymphoma: A Diagnostic Dilemma
PRESENTER: Bashar Hmoud
PRESENTER (INSTITUTION ONLY): University of Texas Medical Branch
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction: Hodgkin’s lymphoma is a disease that arises from B cells in the germinal or post-germinal
center. It accounts for 11% of all lymphomas, and 0.55% of all cancers in the developed world. Involvement of the liver
is not rare, though having liver involvement as part of the initial manifestations is uncommon, and occurs in less than
4% of the patients. Obstructive jaundice is most commonly caused by a mass compression of the common bile duct,
though other causes may include lymphoma infiltration and vanishing bile duct syndrome.
Case Presentation: The patient is a 43-year-old male with past medical history of HIV/AIDS, hypertension completely
treated latent syphilis, and a recently diagnosed Hodgkin’s lymphoma nodular sclerosis type, who was referred from
his HIV clinic for diarrhea and yellowish discoloration of the sclera. He reported starting anti-retroviral therapy a month
prior to presentation, and he developed watery diarrhea 1-2 weeks after initiating therapy. Along with the diarrhea, the
patient developed gradually worsening yellowish discoloration of the skin and eyes, associated with cola-colored
urine. The initial work-up showed severe hyperbilirubinemia mainly conjugated, though imaging with ultrasound of the
liver, followed by contrasted abdominal CT and MRCP, were all within normal limits. The patient had a liver biopsy,
which showed lymphoma involvement of the liver.
Discussion: In a previous case series, the prevalence of initial liver involvement with lymphoma was 7.4%, with 1.4%
of the cases having liver disease as the presenting symptom. It was more associated with the more aggressive
lymphocytic depletion and mixed cellularity histologic types. In this case, the patient was diagnosed with lymphoma
involvement of the liver, and improved on treatment with chemotherapy. Vanishing bile duct syndrome is a rare
disorder that can be a paraneoplastic disorder associated with Hodgkin’s disease. The diagnosis can be delayed, as
usually, patients have normal cholangiography, and the ductopenia might be subtle on the liver biopsy.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Bashar Hmoud : ACG Non-Member
Sarpreet Basra : ACG Member
Andrea Duchini : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: [No Comments]|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No Comments]|James
Vecchio: [No Comments]
CONTROL ID: 1741981
TITLE: Neutrocytic Ascites and Clostridium difficile-Associated Diarrhea: Should Patients Be Treated Empirically for
Spontaneous Bacterial Peritonitis?
PRESENTER: Brent Lacey
PRESENTER (INSTITUTION ONLY): Naval Medical Center San Diego
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Case 1: A 68-year-old woman with cryptogenic cirrhosis presented with new high SAAG neutrocytic ascites
(PMN: 421) and Clostridium difficile-associated diarrhea (CDAD). She was treated empirically with oral vancomycin
and five days of cefotaxime. Ascitic fluid cultures were negative, and her diarrhea resolved.
Case 2: A 58 -year-old woman with hepatitis C cirrhosis presented with high SAAG neutrocytic ascites (PMN: 778)
and severe CDAD. She was treated with iv metronidazole and oral vancomycin, as well as cefotaxime. At 48 hours,
ascitic fluid cultures were preliminarily negative, and cefotaxime was stopped. Final ascitic fluid cultures remained
negative, and she recovered.
Discussion: The standard treatment for spontaneous bacterial peritonitis (SBP) is early initiation of antibiotics and
albumin after performing a diagnostic paracentesis. However, in CDAD, early discontinuation of broad-spectrum
antibiotics is critical. In our two patients, this led to a therapeutic dilemma that required us to consider whether to
discontinue antibiotics early in patients undergoing empiric treatment for SBP. Ascites is a common finding in cases of
CDAD, up to nearly 80% in some case series (1,2,3,4). The overall specificity of ascites is low, as it may be seen in a
variety of conditions (3,4). To our knowledge, this is the first report of a scenario of CDAD in a patient with cirrhosis
and ascites with SAAG >1.1, with a high neutrophil count (>250/mL).
Conclusion: Cirrhotic patients with CDAD may have culture-negative neutrocytic ascites from colitis alone. Based on
our experiences, it may be reasonable to stop empiric treatment of SBP in a patient with high SAAG (>1.1) neutrocytic
(>250/mL) ascites, who has confirmed CDAD, if ascitic cultures are negative at 48 hours.
References:
1. Jafri SF, et al. Ascites Associated with Antibiotic-Associated Pseudomembranous Colitis. Southern Med Jour
996;89(10): 1014-1017.
2. Kirkpatrick ID, et al. Evaluating the CT diagnosis of Clostridium difficile colitis: should CT guide therapy? Am J
Roentgenol. 2001;176(3):635-9.
3. Kawamoto S, et al. Pseudomembranous colitis: spectrum of imaging findings with clinical and pathologic
correlation. Radiographics. 1999;19(4):887-97.
4.Boland GW, et al. Clostridium difficile colitis: correlation of CT findings with severity of clinical disease. Clin Radiol
1995;50(3):153-6.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Brent Lacey : ACG Member
Kishore Gaddipati : ACG Member
Brett Partridge : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: [No Comments]|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No Comments]|James
Vecchio: [No Comments]
CONTROL ID: 1742249
TITLE: Myositis Portends Primary Biliary Cirrhosis: A Case Series
PRESENTER: Carrie Wong
PRESENTER (INSTITUTION ONLY): Beth Israel Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Although the presence of anti-mitochondrial antibody (AMA) is 98% specific for primary biliary cirrhosis
(PBC), AMA is associated with other autoimmune diseases, including inflammatory myopathies. A recent study in
Brain found 23 case reports of concurrent PBC and polymyositis (PM), and only one of autoimmune hepatitis (AIH)PBC overlap with PM. We present two patients from our institution with AIH-PBC overlap and PM, and discuss their
management.
Case 1: A 60-year-old woman with sicca syndrome was referred to us for persistently elevated aminotransferase
values, immunoglobulin M (IgM) (666mg/dL), and immunoglobulin G (IgG) (1,950 mg/dL). A liver biopsy confirmed
Scheuer stage I PBC with AIH, and she was started on prednisone and ursodiol. Concurrent to her PBC diagnosis and
before prednisone therapy, she developed progressive proximal muscle weakness. Muscle biopsy, electromyography,
and elevated muscle enzyme levels suggested PM. On prednisone, her liver enzyme levels normalized while muscle
strength responded to several months of intermittent intravenous immunoglobulin. Three years later, she developed
diastolic heart failure, which improved on diltiazem. Her disease was complicated by severe osteoporosis, treated with
zoledronic acid, calcium, and vitamin D. Currently, she is doing well on ursodiol 500 mg daily, and prednisone five mg
every other day.
Case 2: A 58-year-old man presented to a neurologist after one year of truncal weakness. His muscle biopsy, elevated
muscle enzymes, and symptoms suggested PM. He responded to prednisone, but was subsequently referred to
hepatology for persistently elevated liver test results (AST 89, ALT 99, ALK PHOS 305). AMA (1:160), IgG (2350
mg/dL) and IgM (402 mg/dL) were elevated. Liver biopsy confirmed stage I PBC with confluent necrosis, suggesting
AIH overlap. Prednisone 60 mg daily and ursodiol 500 mg twice-a-day were initiated. After three months of treatment,
the patient’s symptoms improved and liver enzyme activity normalized.
Discussion: Although AIH-PBC with PM is an infrequently recognized syndrome, we encountered two such cases. The
natural course of AIH-PBC and PM is unknown, but some studies show that PM with concurrent PBC may have a
more indolent PM with frequent cardiac involvement, as seen in our first patient. Both patients responded to and are
being maintained on prednisone and ursodiol. For PM with AIH, if prednisone treatment alone fails, the addition of
immunosuppressive agents given singly or in combination with corticosteroids may be considered. Since
corticosteroid use may worsen osteoporosis associated with advanced PBC, assessment of bone density with the
potential use of bisphosphonates may be valuable.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Simi Singh : ACG Non-Member
Carrie Wong : ACG Member
Lan Wang : ACG Non-Member
Daniel Macgowan : ACG Non-Member
Harry Fischer : ACG Non-Member
Neil Theise : ACG Non-Member
Henry Bodenheimer : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: [No Comments]|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No Comments]|James
Vecchio: [No Comments]
CONTROL ID: 1742333
TITLE: Trazodone and Gabapentin Drug-Induced Liver Injury
PRESENTER: Chau Che
PRESENTER (INSTITUTION ONLY): New York Medical College
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Trazodone and gabapentin are commonly used treatments. We report a rare case of trazodone and
gabapentin-induced liver injury.
Case: A 40-year-old woman with a history of depression presented jaundice. She had no other complaints. The
patient denied risk factors for acute and chronic liver disease. She had been taking trazodone 50 mg daily for the past
five years. The only concomitant medication was gabapentin, which she had been taking for many months, for pain.
She had no family history of liver or autoimmune diseases. Physical exam was normal, with the exception of jaundice.
Laboratory tests showed: total bilirubin 33.7 mg/dL, direct bilirubin 23.9 mg/dL, ALT 582 U/L, AST 774 U/L, alkaline
phosphatase 142 U/L, and INR 1.64. There was no evidence of infection from hepatitis A, B, C, or E. Antinuclear Ab,
anti-smooth muscle Ab, anti-mitochondrial Ab, anti-LKM, and anti-SLA were negative. Quantitative immunoglobulins,
ceruloplasmin, hemochromatosis gene analysis, and alpha-1-antitrypsin were normal or negative. Ultrasound showed
a normal liver with patent vessels. Liver biopsy showed chronic hepatitis, markedly active with multifocal necrosis,
focal parenchymal collapse, and bridging necrosis with mild portal fibrosis. There was a dense mononuclear portal
infiltrate with eosinophils and widespread swelling of hepatocytes. Trazodone and gabapentin were discontinued. The
patient was treated with methylprednisolone 32 mg intravenously (IV) daily. After five days of IV steroids, treatment
was changed to prednisone 40 mg per day. Within one month, the liver chemistries had normalized. Prednisone was
successfully tapered off. Liver chemistries remained normal.
Discussion: Although our patient was steroid responsive, given her normal autoimmune markers, it is likely that our
patient had drug-induced liver injury (DILI) from either trazodone or gabapentin. The reversal of symptoms upon
discontinuation of medications supports the diagnosis of drug-induced etiology. DILI from trazodone was reported in
six case reports. One individual required liver transplant. Clinically, all patients presented with acute hepatitis.
Histologically, acute hepatitis was seen in five cases, and chronic hepatitis was seen in one case. Gabapentin was
reported to cause cholestasis in two case reports. Despite the small number of reported cases of hepatotoxicity,
trazodone and gabapentin are known causes of liver injury, and clinicians should be aware of this possibility.
Methods: NA
Results: NA
Conclusion: NA
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Chau Che : ACG Member
Roxana Bodin : ACG Non-Member
David Wolf : ACG Member
(No Image Selected)
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AVERAGE SCORE: 4.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: syntax errors (missing words)|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No
Comments]|James Vecchio: [No Comments]
CONTROL ID: 1742478
TITLE: Transjugular Intrahepatic Portosystemic Shunt (TIPS) for the Treatment of Anorectal Varices
PRESENTER: Juan Blum Guzman
PRESENTER (INSTITUTION ONLY): Florida Hospital
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Despite the high prevalence of anorectal varices in portal hypertension, serious hemorrhage is quite rare,
but may be fatal. Although several techniques for treating acute bleeding have been reported, the optimal therapeutic
management has not been established. We report a patient with severe recurrent rectal bleeding from anorectal
varices successfully treated by a transjugular intrahepatic portosystemic shunt (TIPS).
A 53-year-old man with known history of hepatitis C-induced liver cirrhosis, listed for possible liver transplantation and
prior decompensation in the form of esophageal variceal bleed maintained on beta-blockers, presented to the
emergency department with the chief complaint of rectal bleeding for one week's duration, associated with weakness,
dizziness, shortness of breath, and generalized abdominal pain. On admission, labs showed: WBC 1.3, hb 10.4, hct
31.4, INR 1.5, total bilirubin 1.4, alkaline phos 136, ALT 43, AST 70.
CT abdomen and pelvis performed the day of admission revealed: diffuse cirrhosis without hepatic lesion,
splenomegaly, large-caliber gonadal varices that extend to the pelvis and surround the rectum, as well as concentric
thickening of the rectum. Due to presentation and findings, gastroenterology was consulted. EGD showed grade 2
esophageal varices without stigmata of recent bleeding, and gastric antral vascular ectasia (GAVE) without active
bleeding. Colonoscopy showed very large rectal varices. One column had a small mucosal hemorrhage present, no
active bleeding esd present, and a nonbleeding cecal AVM.
After extensive discussion between the hepatology and GI departments about options for treatment, it was decided to
pursue transjugular intrahepatic portal systemic shunt (TIPS) to relieve portal pressure causing the rectal varices. The
patient underwent successful TIPS procedure, performed by the interventional radiology department. Contrast
injections during the examination demonstrated hepatofugal flow in the portal vein. The patient was also noted to have
splenorenal shunting, as well as massive inferior mesenteric vein filling rectal varices. A Rosen wire was placed. The
tract was dilated to 8 mm. A 10-mm x 80-mm covered VIATORR stent was placed. Follow-up pressures demonstrated
a mean portal pressure of 29 mmHg with a central venous pressure of 29/22, with a mean of 25 mmHg. There
remained flow in the inferior mesenteric vein; however, it subjectively appeared to be slower. After the procedure, the
patient was discharged to be followed closely as an outpatient. A follow-up colonoscopy was performed two months
after TIPS procedure. showing one cord of rectal varices, approximately 75% improved since prior colonoscopy, and
small internal hemorrhoids.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Juan Blum Guzman : ACG Non-Member
Kawtar Alkhalloufi : ACG Non-Member
Zahid Vahora : ACG Non-Member
Kamran Qureshi : ACG Non-Member
Hicham Khallafi : ACG Non-Member
Edula Raja : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: [No Comments]|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No Comments]|James
Vecchio: [No Comments]
CONTROL ID: 1742631
TITLE: An Unusual Cause of Ascites
PRESENTER: Matthew Kutner
PRESENTER (INSTITUTION ONLY): Bethi Israel Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 63-year-old African-American man with a history of alcoholism and hepatitis C was admitted with fever and
abdominal distention. A paracentesis was performed, and ascitic fluid analysis demonstrated a total leukocyte count of
4940u/l, with 41% neutrophils. The serum albumin-ascitic gradient (SAAG) was not calculated. He was diagnosed with
spontaneous bacterial peritonitis (SBP), given a five-day course of cefotaxime, then discharged home. Two days
following discharge, the patient developed malaise, with worsening abdominal distention. After two weeks of
progressive symptoms, he returned to the emergency room.
Repeat paracentesis was significant for leukocytes of 1995 u/l with 7% neutrophils and 79% lymphocytes, fluid
albumin of 3.0 g/dl, and protein 8.3 g/dl. The SAAG was calculated as 0.7. Quantiferon Tb Gold results were
indeterminate, and alpha-fetoprotein was normal, at 2.4 ng/ml. MRI of the abdomen illustrated a 1.1 x 1.2 cm
hypervascular liver lesion, but no cirrhotic morphology. Random liver biopsy showed markedly active chronic hepatitis,
with trichome and reticulin stains positive for mild, focal portal fibrosis, inconsistent with cirrhosis. PAS-D stain for
mycobacterium species was negative. The patient was discharged home with scheduled follow-up in hepatology clinic,
which he did not attend. Six weeks following discharge, the ascitic fluid culture grew Mycobacterium mucogenicum.
The patient could not be reached, despite multiple attempts at contact.
Initially named Mycobacterium chelonae-like organism, M. mucogenicum was the agent responsible for the 1976 and
1978 peritonitis outbreaks in two peritoneal dialysis centers in the United States. Since its detection, M. mucogenicum
has been widely identified, and linked to contaminated water. It is the most commonly isolated Mycobacterium species
from environmental water sources. Members of the group have been discovered within both public and hospital water
systems, where their ability to endure chlorination, disinfectants, and extreme temperatures have allowed them to
persist. It is unclear how our patient came to be infected.
In conclusion, we present an unusual case of ascites due to M. mucogenicum. Although rare, this organism should be
included in the differential diagnosis when evaluating a patient with new ascites, as this family of organisms has
become more clinically significant with the use of immunosuppressive agents. Even when a common etiology seems
likely (i.e. transudative ascites due to cirrhosis in a patient with known chronic liver diseases), a thorough
understanding of the wide differential diagnosis of ascites and complete fluid analysis is essential to determine its
etiology.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Matthew Kutner : ACG Non-Member
Lan Wang : ACG Member
Jason Rubinov : ACG Non-Member
Andrew Korman : ACG Non-Member
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AVERAGE SCORE: 4
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: [No Comments]|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No Comments]|James
Vecchio: [No Comments]
CONTROL ID: 1742726
TITLE: Neutrocytic Ascites and Clostridium Difficile-Associated Diarrhea: Should Patients Be Treated Empirically for
Spontaneous Bacterial Peritonitis?
PRESENTER: Brent Lacey
PRESENTER (INSTITUTION ONLY): Naval Medical Center, San Diego
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Case 1: A 68 year-old woman with cryptogenic cirrhosis presented with new high SAAG neutrocytic ascites
(PMN: 421) and Clostridium difficile-associated diarrhea (CDAD). She was treated empirically with oral vancomycin
and five days of cefotaxime. Ascitic fluid cultures were negative, and her diarrhea resolved.
Case 2: A 58-year-old woman with hepatitis C cirrhosis presented with high SAAG neutrocytic ascites (PMN: 778) and
severe CDAD. She was treated with iv metronidazole and oral vancomycin, as well as cefotaxime. At 48 hours, ascitic
fluid cultures were preliminarily negative, and cefotaxime was stopped. Final ascitic fluid cultures remained negative,
and she recovered.
The standard treatment for spontaneous bacterial peritonitis (SBP) is early initiation of antibiotics and albumin after
performing a diagnostic paracentesis. However, in CDAD, early discontinuation of broad-spectrum antibiotics is
critical. In our two patients, this led to a therapeutic dilemma that required us to consider whether to discontinue
antibiotics early in patients undergoing empiric treatment for SBP. Ascites is a common finding in cases of CDAD, up
to nearly 80% in some case series (1,2,3,4). The overall specificity of ascites is low as it may be seen in a variety of
conditions (3,4). To our knowledge, this is the first report of a scenario of CDAD in a patient with cirrhosis and ascites
with SAAG >1.1 with a high neutrophil count (>250/mL). Cirrhotic patients with CDAD may have culture-negative
neutrocytic ascites from colitis alone. Based on our experiences, it may be reasonable to stop empiric treatment of
SBP in a patient with high SAAG (>1.1) neutrocytic (>250/mL) ascites who has confirmed CDAD if ascitic cultures are
negative at 48 hours.
References
1. Jafri SF, et al. Ascites Associated with Antibiotic-Associated Pseudomembranous Colitis. Southern Med Jour
1996;89:1014-1017.
2. Kirkpatrick ID, et al. Evaluating the CT diagnosis of Clostridium difficile colitis: should CT guide therapy? Am J
Roentgenol 2001;176:635-9.
3. Kawamoto S, et al. Pseudomembranous colitis: spectrum of imaging findings with clinical and pathologic
correlation. Radiographics 1999;19:887-97.
4. Boland GW, et al. Clostridium difficile colitis: correlation of CT findings with severity of clinical disease. Clin Radiol
1995;50:153-6.
Methods: n/a
Results: n/a
Conclusion: n/a
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Brent Lacey : ACG Member
Kishore Gaddipati : ACG Member
Brett Partridge : ACG Member
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AVERAGE SCORE: 4.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: [No Comments]|Selvi Thirumurthi: There are 2 clinical vignettes that address this topic|Renu
Umashanker: [No Comments]|James Vecchio: [No Comments]
CONTROL ID: 1743028
TITLE: De Novo Malignant Melanoma Presenting as Fulminant Hepatic Failure: A Case Report
PRESENTER: Mohsen Khan
PRESENTER (INSTITUTION ONLY): Advocate Lutheran General Department of Gastroenterology
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: We report a case of fulminant hepatic failure as the initial presentation of metastatic melanoma. An 82-yearold non-alcoholic male with a history of dementia and no known liver disease presented to the emergency department
with abdominal pain, vomiting, and diarrhea. Liver chemistries revealed an aspartate aminotransferase 400 unit/L,
alanine aminotransferase 119 unit/L, alkaline phosphatase 465 unit/L, total bilirubin 2.9 gm/dL, conjugated bilirubin 2.1
gm/dL, total protein 4.8 gm/dL, and serum LDH of 4,565 unit/L. Sonography of the abdomen revealed a hypoechoic
liver, gallbladder wall thickening, with normal bile ducts. A portal hepatic duplex was suggestive of portal hypertension.
An MRCP, as well as laboratory work-up for underlying chronic liver disease, was unremarkable. The patient
continued to have worsening abdominal pain, abdominal distension, and jaundice with a maximal bilirubin of
18.7gm/dl, accompanied by encephalopathy and worsening coagulopathy. Liver biopsy demonstrated a liver
parenchyma completely replaced by metastatic melanoma, with marked cholestasis and hepatocyte necrosis. Due to
the patient's underlying co-morbid conditions and rapid deterioration, the family decided to pursue hospice care.
Malignant melanoma is a common malignancy that has the potential to metastasize to any site, with liver involvement
in one third of all cases. While acute hepatic failure has been reported with subsequent infiltration of the liver from
lymphoma, breast, gastric, and lung cancers, there have only been a few cases reported in the literature with
metastatic melanoma of unknown origin initially presenting as fulminant hepatic failure.
Methods: NA
Results: NA
Conclusion: NA
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Mohsen Khan : ACG Non-Member
Andrew Mazulis : ACG Member
Catherine Ly : ACG Member
Kenneth O'Riordan : ACG Member
Suhair Alsalihi : ACG Non-Member
Michael Mihalov : ACG Non-Member
Fig 1
Histology reveals cholestatic hepatic tissue with a subtle infiltration by deeply pigmented, hepatoid cells which clearly
mark as melanocytes.
Fig 2
IMAGE CAPTION: Fig 1
Histology reveals cholestatic hepatic tissue with a subtle infiltration by deeply pigmented, hepatoid cells which clearly
mark as melanocytes. Fig 2
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AVERAGE SCORE: 4.25
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Vecchio: [No Comments]
CONTROL ID: 1743148
TITLE: Don’t Oversee It when It Happens With HCV: A Case of HCV-Induced Porphyria Cutanea Tarda
PRESENTER: Raphael Quansah
PRESENTER (INSTITUTION ONLY): Texas Tech Health Science Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 47-year-old male patient presented to the emergency department complaining of fever, chills, and swelling
of his right thumb for one week. Chart review revealed multiple hospitalizations for similar presentations, which were
treated for cellulitis and abscesses to hands, forearm, and face. His past medical history included: HIV/AIDS, hepatitis
C (HCV), IV drug abuse, and CMV retinitis. Physical examination revealed fever (39.0 C), circumferential swelling, and
redness of the right thumb distal phalanx. Face, forearm, and backs of both hands showed multiple blisters, bullae,
hypo, and hyperpigmentation; scarring and pseudoscleroderma of the sun-exposed skin areas (Fig. A, B & C).
Cryoglobulin and scleroderma work-up were negative; ferritin level 1800 ng/ml elevated. Total urine porphyrins
(2223.6mg/g creatinine.), uroporphyrins (1000.9mg/g creatinine), and Carboxylated uroporphyrins were increased.
Coproporphyrin level was normal. Images of the thumb confirmed the diagnosis of recurrent osteomyelitis. The
diagnosis of HCV-induced Porphyria Cutanea Tarda (PCT) was established. PCT that is known to be associated with
hepatitis C is the main contributing factor for the previous presentations of cellulitis, abscesses, and the recurrent
osteomyelitis. The patient was referred to the hematology clinic for scheduled phlebotomy. Due to his history of CMV
retinitis, hydroxychloroquine was not an option for therapy.
PCT is the most common presentation of porphyrias, and is often misdiagnosed; 80% is usually sporadic, and occurs
due to a functional deficiency of the hepatic uroporphyrinogen decarboxylase enzyme (UROD). A strong association
between HCV and PCT was first reported in 1992; review of the literature revealed an associated prevalence of 50%
of HCV in PCT patients.
HCV is a cytopathic virus, which can decompartmentalize iron from hepatocytes
leading to free iron that can uncouple the cytochrome P450 system, leading to formation of oxygen radicals, which are
known to reduce UROD activity. Furthermore, HCV decreases hepatic production of glutathione, and therefore
compromises the ability to reduce oxidized uroporphyrins. HCV induces dysregulation of hepatic production of
Hepcidin, leading to unregulated absorption of intestinal iron.
The clinical link of HCV and recurrent skin infection mediated by the presence of PCT, initially detected by physicians
and medical staff, is essential to allow delivering an adequate therapy and secondary prevention of recurrent
hospitalizations.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Raphael Quansah : ACG Non-Member
Sarmad Said : ACG Non-Member
Jorge Bizet : ACG Non-Member
Richard Guerrero : ACG Member
IMAGE CAPTION:
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AVERAGE SCORE: 4.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: [No Comments]|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No Comments]|James
Vecchio: [No Comments]
CONTROL ID: 1743174
TITLE: Retroperitoneal Bleeding: An Odd Presentation for Hepatocellular Carcinoma (HCC)
PRESENTER: Leonard Philo
PRESENTER (INSTITUTION ONLY): NMCSD
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 55-year-old man with a history of alcohol abuse presented with acute, severe left-flank pain that occurred
at rest. He denied any trauma, sick contacts, fevers, dysuria, hematuria, melena, constipation, weight loss, chest pain,
shortness of breath, or anticoagulation use. Physical exam was remarkable for tachycardia, and few stigmata of
chronic liver disease. He had a macrocytic anemia, thrombocytopenia, and AST/ALT ratio of 131:97, with normal
BUN, creatinine, and INR. A CT scan revealed a retroperitoneal hemorrhage with evidence of active extravasation and
a 4-cm heterogenous adrenal mass. (Picture) Two hepatic lesions (1.7 and 3.0 cm), one right adrenal lesion, and an
intrahepatic IVC protruding tumor were also identified. Interventional radiology embolized the left adrenal artery
successfully, with no further bleeding. Work-up for the adrenal and hepatic masses discovered an AFP of 147, positive
HCVAB, and normal metanephrines, cortisol, aldosterone, and renin. A liver biopsy revealed HCC in a background of
cirrhosis.
Symptoms from adrenal metastases of HCC are rare, despite the adrenal gland being the 4th most common
metastatic site. There is a paucity of North American literature detailing cases or management of HCC adrenal
metastases. A literature search has revealed predominantly cases from Asia. The largest retrospective review,
published out of Hong Kong, on metastatic adrenal tumors, had 464 patients, of which 4.3% presented with
symptoms, and 4.7% of the lesions were HCC metastases. One large Japanese review of 342 HCC patients with
extrahepatic metastasis analyzed the clinical features, prognoses, and treatments. The average age at diagnosis was
66.9 +/- 9 years, and 8.8% of metastases were adrenal. 82% of patients had a primary HCC lesion identified when the
extrahepatic metastasis was diagnosed. 19% of patients had intrahepatic vascular tumor invasion, with 3.4 % having
IVC invasion. Treatment options included resection, chemotherapy, irradiation, TACE, and percutaneous ablation.
Our case demonstrates the efficacy of IR embolization for bleeding from adrenal HCC metastases. Extrahepatic
metastases are not the usual cause of death in these patients, but do portend the aggressiveness of HCC. Our goal is
to increase awareness of an uncommon complication of metastatic HCC. As more cases are treated and reported,
comparisons can be made between treatment modalities and improve patient outcomes.
Methods: NA
Results: NA
Conclusion: NA
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Leonard Philo : ACG Member
Sharon Chien : ACG Non-Member
Susan Chu : ACG Member
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AVERAGE SCORE: 4
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: [No Comments]|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No Comments]|James
Vecchio: [No Comments]
CONTROL ID: 1743239
TITLE: A Rare Case of Spontaneous Tumor Lysis Syndrome in a Patient with Hepatitis C and B-Cell Lymphoma
PRESENTER: Anita Bakshi
PRESENTER (INSTITUTION ONLY): George Washington University
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Individuals with chronic hepatitis C have an increased risk for development of non-Hodgkin’s lymphoma,
most commonly B-cell subtypes. Management of hepatitis C-infected patients with B-cell lymphoma is similar to that of
patients who are hepatitis C-negative. Tumor lysis syndrome is an oncologic emergency characterized by a spectrum
of metabolic abnormalities that typically occur after initiating cytoreductive therapy in patients with rapidly proliferative
hematopoietic malignancies. Spontaneous tumor lysis syndrome is very rare and of unknown etiology. This is the first
case of an individual with hepatitis C presenting with tumor lysis syndrome from B-cell lymphoma prior to
administration of chemotherapy.
A 63-year-old woman with known hepatitis C (genotype 1a, treatment naïve) with compensated cirrhosis presented
with cervical and submandibular adenopathy. A CT scan revealed bulky para-aortic and periportal lymphadenopathy.
Fine needle aspirate of a cervical lymph node was nondiagnostic. Flow cytometry of the aspirate was suggestive of a
possible lymphoma. Five days later, she presented to the emergency department with progressive fatigue, myalgias,
anorexia, and dyspnea. She was found to have fluid-responsive hypotension with metabolic abnormalities (potassium
6.7 mEq/L, phosphorus 6.7 mg/dL, uric acid 14.7 mg/dL) and renal insufficiency (creatinine 2.1 mg/dL). Given her
lymphadenopathy, hyperkalemia, hyperuricemia, kidney injury, and elevated LDH, the oncologist diagnosed
spontaneous tumor lysis. She was started on aggressive hydration, rasburicase, allopurinol, and kayexylate. Bone
marrow biopsy showed an infiltrate of predominantly intermediate to large sized cells. Immunohistochemical staining
revealed neoplastic B cells (CD20 positive) that were positive for CD23, BCL2, BCL6, and MUM1. Greater than 90%
of neoplastic cells were Ki67 positive, indicative of a high proliferative rate associated with a high-grade lymphoma. A
lymph node biopsy revealed diffuse large B cell lymphoma. Chemotherapy was initiated. However, she continued to
decline with development of progressive edema, dyspnea, and persistent electrolyte abnormalities. The following day,
she developed septic shock with gram negative rods. She succumbed to multiorgan system failure.
Chronic hepatitis C is associated with an increased risk for non-Hodgkin’s lymphoma. However, spontaneous tumor
lysis syndrome is a very rare entity, and is associated with rapid tumor progression with poor prognosis. This
syndrome has never been reported in a patient with hepatitis C and B-cell lymphoma. It t is critical that physicians are
aware of the potential occurrence, to ensure prompt recognition and aggressive treatment.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Anita Bakshi : ACG Member
Lakshmi Lattimer : ACG Member
Erica DaCosta : ACG Non-Member
Marie Borum : ACG Member
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AVERAGE SCORE: 3.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: [No Comments]|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No Comments]|James
Vecchio: [No Comments]
CONTROL ID: 1743247
TITLE: Pasteurella multocida Sepsis in Hepatitis C Infected Patient
Jain J. MD, Devathi S. MD, Gajjala J. MD
Division of Internal Medicine, Howard University Hospital
PRESENTER: Juhi Jain
PRESENTER (INSTITUTION ONLY): howard university hospital
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Pasteurella multocida is a gram negative baccilli that is a common commensal in the oropharnyx and GI
tract of domestic animals especially dogs and cats. Infections range from local soft tissue infections, cellulitis to
systemic infections. Pasteurella multocida may act as an opportunistic pathogen causing bacteremia in patients with
underlying respiratory tract abnormalities or liver dysfunction, meningitis in the very young or elderly, or septic arthritis
in damaged tissue. Pasteurella sepsis cases are rare and have been reported in patients with underlying liver disease
and immune compromised status. Bite wounds with pasteurella infection have been well studied and reported
however non bite exposure leading to septicemia is rare. Treatment includes beta lactam antibiotics.
We report a case of a 58 year old female with hepatitis C, liver cirrhosis and esophageal varices who presented to ICU
with swelling and pain of the right leg, fever and chills since 1 day. On examination patient had cellulitis of lower
extremity with a bullous lesion on the right thigh and hyperpigmentation, chronic skin changes on left leg. On further
probing patient gave history of having a pet dog licking her legs occasionally.
Patient was started on broad spectrum antibiotics and pressor agents for hypotension. 2 out of 2 blood cultures drawn
on admission grew Pasturella Multocida. Antibiotics were switched to Unasyn and Clindamycin. Patient developed
new bullous lesions on the leg with worsening respiratory status and liver function. On day 5 patient had to be
intubated for acute respiratory distress. Patient continued to worsened with increasing leucocytosis, worsening liver
function, acute renal failure, thrombocytopenia, coagulopathy and multiorgan failure. Acute renal failure required
dialysis however patient could not get vascular access due to coagulopathy and died on day 11.
This case is unique because of culmination of the three factors - underlying liver disease, non invasive animal
exposure with dog licks and Pasteurella sepsis leading to fatal outcome due to poor hepatic reserves. This case
illustrates that infection with P. multocida can result from casual contact with household pets and does not require a
specific animal bite or scratch trauma. High index of suspicion is required by clinicians in patients with impaired host
defenses and animal contact and should be treated promptly with appropriate antibiotics as mortality rates are 77% in
cases of Pasteurella sepsis in liver disease patients.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Juhi Jain : ACG Non-Member
(No Image Selected)
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AVERAGE SCORE: 3.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: [No Comments]|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No Comments]|James
Vecchio: [No Comments]
CONTROL ID: 1743264
TITLE: Altered Mental Status In A Patient With Liver Cirrhosis: Its Not Always The Liver
PRESENTER: Saleh Elwir
PRESENTER (INSTITUTION ONLY): Hershey Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 55-year-old morbidly obese male patient who is status post gastric bypass surgery and liver cirrhosis
secondary to non-alcoholic steatohepatitis (NASH) was admitted to the hospital in the setting of upper gastrointestinal
(GI) bleed. Endoscopic evaluation revealed that the cause of the bleeding was related to dehiscence of the staple line
of a previous gastric bypass surgery, with associated friable mucosa. Patient was treated medically, and his GI
bleeding stopped. Over the course of the next few days, the patient became encephalopathic, requiring intubation.
This was thought to be due to a combination of renal failure and sepsis, as the patient’s blood cultures were positive
for coagulase-negative Staphylococcus. Despite treatment with the appropriate antibiotics, lactulose, rifaximin, and the
resolution of the patient’s renal failure, his mental status failed to improve. An MRI of the brain was significant for
evidence of posterior reversible encephalopathy syndrome (PRES). Supportive care was continued, and the patient
was discharged to a long-term care facility, where his symptoms slowly improved over the course of the next few
months. PRES is seen in patients after liver transplantation, often as a result of the use of calcineurin inhibitors, and is
seen in patients with elevated blood pressures and renal failure. Failure of encephalopathy resolution in patients with
liver cirrhosis after reversal of possible precipitating factors should prompt consideration of less common factors that
can result in an altered mental status.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Saleh Elwir : ACG Non-Member
Lisa Yoo : ACG Non-Member
Thomas Riley : ACG Member
IMAGE CAPTION:
(no table selected)
AVERAGE SCORE: 4.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: [No Comments]|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No Comments]|James
Vecchio: [No Comments]
CONTROL ID: 1743316
TITLE: Ruptured Hepatocellular Carcinoma of Caudate Lobe Causing Hematoma of Lesser Sac and Hemoperitoneum
PRESENTER: Yezaz Ghouri
PRESENTER (INSTITUTION ONLY): University of Texas Health Science Center at Houston
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Case Report: A 53-year-old man with chronic hepatitis C and alcoholic cirrhosis presented with sudden
onset acute abdominal pain, abdominal distension, nausea, and vomiting. Upon presentation, he had declining BP,
but stabilized after fluid resuscitation. On physical exam, he was found to have abdominal tenderness and guarding.
Labs showed Hemoglobin (Hb) of 10.9 g/dl (baseline 13.5), platelets: 114 /mm3, INR: 1.5, albumin: 2.5 g/dl, total
bilirubin: 1.3 g/dL, and AST: 78 U/L. Diagnostic paracentesis showed hemorhagic ascitic fluid with >2 million
RBC’s/mm3, 735 WBC’s with a SAAG >1.1. Triple–phase CT abdomen showed a cirrhotic liver with a 3.1-cm diameter
lesion in caudate lobe (Figure 1). Two intrabdominal fluid collections of different densities were identified; one
consistent with hemoperitoneum extending from caudate lobe to the lesser sac, and a second consistent with ascites
in the lower quadrants. The Surgical team elected to conservatively manage the patient, since he was then
hemodynamically stable with a stable Hb. A week later, an MRI confirmed a 3.3-cm enhancing lesion consistent with
ruptured hepatocellular carcinoma (HCC) in the caudate lobe. He underwent successful transarterial
chemoembolization (TACE) with doxorubicin beads about two months after his bleeding episode. Following the
procedure, he has been seen in clinic and has not had any acute abdominal complaints over last four months. The
hematoma has regressed in size on imaging.
Discussion: Spontaneous rupture of HCC is associated with a high inpatient mortality of 25-75%. Hematoma of lesser
sac as a consequence of a ruptured HCC with hemoperitoneum is a relatively rare presentation. Surgical resection of
tumor is associated with higher risk of complications, especially in patients with concomitant cirrhosis. Radiofrequency
ablation is technically difficult, due to the deep location of the tumor. TACE is the preferred loco-regional approach for
tumor in caudate lobe, with good rate of success in controlling bleeding.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Yezaz Ghouri : ACG Non-Member
Katherine Jelinek : ACG Member
Victor Machicao : ACG Non-Member
Figure 1: CT abdomen with contrast showing cirrhotic liver with heterogeneously enhancing 3.1cm ruptured lesion
within the caudate lobe with hematoma of the lesser sac.
IMAGE CAPTION: Figure 1: CT abdomen with contrast showing cirrhotic liver with heterogeneously enhancing 3.1cm
ruptured lesion within the caudate lobe with hematoma of the lesser sac.
(no table selected)
AVERAGE SCORE: 3.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Devi Rampertab: [No Comments]|Selvi Thirumurthi: [No Comments]|Renu Umashanker: [No Comments]|James
Vecchio: [No Comments]
CONTROL ID: 1743400
TITLE: Primary Hepatic Rhabdomyosarcoma in a Woman with a History of Autoimmune Hepatitis
PRESENTER: Sonali Paul
PRESENTER (INSTITUTION ONLY): Tufts Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Liver masses comprise of a wide range of diseases, from benign focal lesions to malignant liver tumors.
Liver lesions in healthy people are often found incidentally, and the majority are benign. In patients with cirrhosis or
underlying liver disease, a hepatic lesion often raises the suspicion of malignancy.
We report a case of a 31-year-old woman who presented with a one-month history of epigastric pain radiating to her
right flank, associated with bloating and anorexia. She had a history of autoimmune hepatitis diagnosed 17 years
earlier. A liver biopsy then was consistent with cirrhosis. She was treated initially with prednisone, and maintained on
azathioprine. Her liver function tests had normalized while on treatment. A repeat liver biopsy done nine years after
her initial diagnosis showed only scattered mononuclear cells with no evidence of bile duct damage or fibrosis. Her
exam was notable for tenderness in the right upper quadrant. Liver function tests were mildly elevated, with ALT 50
IU/L, AST 41 IU/L, but normal bilirubin and alkaline phosphatase. Her chemistries, kidney function, complete blood
count, and prothrombin time were unremarkable. A CT scan of the abdomen revealed a large mass (9 x 10 x 8cm)
occupying the right lobe of the liver, with areas of necrosis in addition to portocaval lymphadenopathy. Alphafetoprotein was less than two. A fine needle aspiration of the mass revealed tumor cells positive for myogenin,
synaptophysin, and desmin, and negative for CD99, pankeratins, and myoD1 consistent with a rhabdomyosarcoma. A
follow-up PET Scan showed uptake in multiple bones and in several lymph nodes in the porta hepatitis. The patient
initiated chemotherapy, but her course was complicated by worsening abdominal pain, pancytopenia, and obstructive
jaundice with a rising bilirubin to 8.1 mg/dL. Despite treatment, repeat imaging showed an increase in the size of the
hepatic mass and worsening adenopathy. Four months after diagnosis, her goals of care shifted to comfort, and she
passed away.
Primary hepatic rhabdomyosarcomas are the most common soft-tissue sarcomas among children, but rare in adults,
with only 12 cases described in the literature since 1979. The malignancy is not usually associated with autoimmune
hepatitis. However, there is some evidence to suggest that patients with autoimmune hepatitis are at increased risk for
cancer, specifically non-Hodgkin’s lymphoma, skin cancers, and hepatobiliary tumors. Resection is preferred for
localized hepatic rhabdomyosarcomas, with cure rates as high as 70%. Metastatic disease is treated with
chemotherapy and subsequent radiation for residual disease, but portends a poor prognosis, as seen in this patient,
with cure rates less than 30%.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Sonali Paul : ACG Member
Kanchan Kantekure : ACG Non-Member
Barbara Weinstein : ACG Non-Member
Kathleen Viveiros : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3.67
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1743423
TITLE: Obliterative Portal Venopathy: A Rare Cause of Pre-sinusoidal Portal Hypertension
PRESENTER: Ajish Pillai
PRESENTER (INSTITUTION ONLY): Department of Medicine, Drexel University College of Medicine
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction: Making an etiologic diagnosis in patients with noncirrhotic portal hypertension can often be a
formidable challenge for clinicians. We describe a rare case of pre-sinusoidal intrahepatic portal hypertension.
Case:A 54-year-old man presented with an upper GI bleed. He had a longstanding history of fibrostenotic Crohn’s
disease s/p surgical resections and therapy with various immunomodulating agents. He had a history of massive
splenomegaly and thrombocytopenia (platelets ~40,000), for which he’d been followed by a hematologist without a
definitive diagnosis, despite numerous tests including a bone marrow biopsy. An EGD revealed large, grade four
esophageal varices, for which he underwent several variceal band ligation sessions. Initial CT imaging demonstrated
a non-cirrhotic liver with a 25-cm spleen, patent portal, hepatic and splenic veins, and no ascites. LFT’s were normal,
and an MRCP showed no evidence of PSC. Viral, autoimmune, and genetic etiologies of chronic liver disease were
unrevealing. A transjugular liver biopsy revealed a borderline elevated hepatic venous pressure gradient of 8 mmHg.
Histology showed moderate macrovesicular steatosis (30%) and a NAFLD activity score (NAS) of 3/8. In addition,
there were prominent periportal shunt vessels with muscularization of small portal vein branches and nodular
regenerative hyperplasia changes; all consistent with a diagnosis of “obliterative portal venopathy (OPV).” There was
mild periportal fibrosis (2/4), but no cirrhosis. A full hypercoaguable work-up failed to reveal an underlying clotting
disorder. A partial splenic artery embolization was performed to reduce the spleen volume, prevent recurrent portal
hypertensive bleeding, and improve the patient’s thrombocytopenia. Several weeks post-procedure, his platelet count
rose to the 200,000 range, and there was complete resolution of varices on follow-up EGD. He has since developed
evidence of some thrombosis in the splenic and portal veins, requiring anti-coagulation.
Discussion: OPV has also been termed “hepatoportal sclerosis,” “noncirrhotic intrahepatic portal hypertension,” and
“idiopathic presinusoidal portal hypertension,” a rare etiology of portal hypertension diagnosed by the astute
pathologist, based on specific histologic features. There is usually minimal-to-moderate portal fibrosis, but no cirrhosis
and a patent splenoportal venous axis. The mechanism of disease pathogenesis is unclear, but in our patient, an
autoimmune/inflammatory disease of the gut may predispose to portal bacteremia/pylephlebitis, which may result in
thrombosis, sclerosis, and obstruction of small- and medium-sized portal vein radicals. His long-term exposure to 6
MP/imuran is another putative precipitating factor.
Methods: na
Results: na
Conclusion: na
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Ajish Pillai : ACG Non-Member
Alexander Trebelev : ACG Non-Member
Suganthi Soundararajan : ACG Non-Member
David Sass : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1743434
TITLE: Tibolone-Induced Acute Hepatitis
PRESENTER: Filipe Vilas-Boas
PRESENTER (INSTITUTION ONLY): Centro Hospitalar S. João
PRESENTER (COUNTRY ONLY): Portugal
ABSTRACT BODY:
Purpose: Tibolone is a sinthetic estrogen used to minimize menopause symptoms. It is usually well-tolerated, and liver
toxicity has been previously reported only on one occasion.
A 45-year-old female with an uneventful medical history was taking tibolone 2.5mg/day for six months. She developed
acute hepatitis with hepatocellular pattern (R=12). On routine blood work, the patient was found to have abnormal liver
tests (ALT 600 UI/L, AST 280 UI/L, GGT 400 UI/L e FA 101 UI/L). Bilirubin was normal. At the evaluation in the
hepatology clinic, the patient was asymptomatic, and physical examination was unremarkable. She had no history of
alcohol intake, and denied over-the-counter use of other drugs or herb products.
Tibolone therapy was discontinued, and complementary study was performed.
We excluded viral hepatitis A, B, C, and E. The tests for metabolic liver disease and auto-immunity came back
negative. Abdominal ultrasound showed no abnormal findings.
Liver biopsy was performed, and revealed unspecific reactive hepatitis, compatible with drug-induced injury. After
tibolone discontinuation, liver tests went back to normal in less than one month. CIOMS/RUCAM summed a total of
nine points, assessing the relationship with the drug as highly probable. The fact that this patient had no previous
history of liver disease, the negative complementary study, and the rapid normalization of liver tests after drug
discontinuation, together with the supporting histological proof of toxicity, support the diagnosis of drug-induced liver
injury.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Filipe Vilas-Boas : ACG Non-Member
Susana Lopes : ACG Non-Member
Helena Baldaia : ACG Non-Member
Fátima Carneiro : ACG Non-Member
Guilherme Macedo : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1743612
TITLE: Statin-Induced Autoimmune Hepatitis
PRESENTER: Javad Hazeghi
PRESENTER (INSTITUTION ONLY): Kingsbrook Jewish Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Drug-induced autoimmune hepatitis is one of potential cause of autoimmune hepatitis accompanied by
development of autoantibodies in predisposed patients. A search of the published literature (1950–May 2013)
revealed few case reports of autoimmune hepatitis associated with statins. We report a case of atorvastatin-induced
autoimmune hepatitis
Methods: A 52-year-old Hispanic female with past medical history of diabetes mellitus type II and hypothyroidism was
starting on atorvastatin. Four weeks later laboratory work-up was done and showed elevation in serum
aminotransferase levels. Despite stopping of atorvastatin, liver function tests continue to being worst and patient was
referred to Kingsbrook Jewish Medical Center for admission.
On admission patient was complaining of generalized weakness and yellowish discoloration of the skin. Serum
aminotransferases were about 20 times the upper limit of normal, bilirubin was 18mg/dl, serum viral markers were
negative and computed tomography of the abdomen was unremarkable.
The presence of autoantibodies including antinuclear antibody (ANA), anti-smooth muscle antibody (SMA) and a liver
biopsy were consistent with autoimmune hepatitis. Use of the Naranjo adverse drug reaction probability scale
indicated a possible (score of 2) temporal and causal relationship between the patient’s autoimmune hepatitis and
atorvastatin. Patient was initiated on Prednisone 60mg daily by mouth and she had clinical and laboratory
improvement in two weeks. Prednisone continued for six weeks and aminotransferases and bilirubin level were in
normal range in one month and six months follow up after tapering prednisone.
Results: There is a theory that suggests autoimmune hepatitis can be initiated in genetically predisposed patients by
environmental triggers like viral agents or medications. The onset of drug-induced autoimmune hepatitis can occur
anywhere from 2months to several years after the initiation of the offending medication. Statins-induced liver injury
may cause elevation of transaminases that usually return to normal with holding the medication. In the literature
search we found statin-induced autoimmune hepatitis is being reported in a few cases and generally patients respond
well to steroids in those cases.
Conclusion: In patients presenting with non-specific signs of autoimmune hepatitis, clinician should be vigilant in the
early recognition of statin as a possible causative agent behind this adverse event. Prompt discontinuation of statin
and initiation of corticosteroid is crucial for a positive drug-induced autoimmune hepatitis clinical course with minimal
sequel.
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Javad Hazeghi : ACG Non-Member
Sreedevi Marakatham : ACG Non-Member
Muhamad Hasan : ACG Non-Member
Michael Liu : ACG Non-Member
Sibet Burney : ACG Non-Member
Jean Luc-Franck : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3.33
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1743630
TITLE: A Rare Case of Autochthonous Hepatitis E in United States
PRESENTER: Ekta Gupta
PRESENTER (INSTITUTION ONLY): Washington Hospital Center/ Georgetown University
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction
Hepatitis E virus (HEV) infection is a common cause of acute viral hepatitis in developing countries and is related to
poor water sanitation. Cases in developed countries are very rare and related to either travel to endemic countries or
contact with individuals who have recently visited these areas. Here we describe an interesting case of acute hepatitis
in United States (US) due to autochthonous HEV infection in a patient without any such travel or contact history.
Case Report
40 year old man with known history of irritable bowel syndrome and hypothyroidism was admitted with fever, chills and
malaise and was diagnosed with acute hepatitis. He had recently visited Cape Cod, Massachusetts few weeks prior to
index presentation; however, there was no history of travel outside US. Initial viral hepatitis screen was negative for
Hepatitis A, B and C virus, Cytomegalovirus, Epstein-Barr Virus, Herpes Simplex Virus, Human Immunodeficiency
Virus, West Nile Virus. Titers for Lyme’s disease, Leptospirosis, Ehrlichia and Babesiosis were negative. Liver
ultrasound was unremarkable. Subsequently patient was referred for HEV antibody IgM testing which was positive
hence confirming the diagnosis of acute hepatitis E.
Discussion
The source of the sporadic HEV infection in developed countries remains usually unidentified as in our case. The
usual risk factors of HEV infection including travel abroad or close contact with someone who has traveled to endemic
country were lacking. Zoonotic transmission related to ingestion of raw meat has been proposed, however, our patient
denied any such history. It has been debated that mollusks and shellfish can be potential sources of infection. Even
though our patient did provide history of swimming in local pond during his visit to Cape Cod, it remains uncertain if
that can be a potential source of infection. Ingestion of imported contaminated food could be an alternative
explanation; however, our patient denied consumption of any such food or any recent change in dietary habits around
the time of infection.
Conclusion
This case highlights that even in developed countries like United States, sporadic cases of HEV related to
autochthonous infection is possible and patients with initial negative routine hepatitis tests should be screened for
hepatitis E, even in the absence of travel history.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: Yes
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Ekta Gupta : ACG Member
Won Cho : ACG Member
Jacqueline Laurin : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3.67
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1743669
TITLE: Subacute Budd-Chiari Syndrome Presenting in a 32-year old African American Woman with Concomitant
Spontaneous Bacterial Peritonitis and Underlying Antiphospholipid Antibody Syndrome
PRESENTER: Nina Ahuja
PRESENTER (INSTITUTION ONLY): UMDNJ
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Background
Budd-Chiari Syndrome is an uncommon clinical condition caused by either thrombotic or non-thrombotic occlusion to
the hepatic venous outflow tract. It occurs most frequently in women in the third or fourth decade of life. This case
highlights subacute Budd-Chiari Syndrome in a young African American woman.
Case
This is a 32 year-old African American woman with a past medical history of mixed connective tissue disease,
systemic lupus erythematosus, and scleroderma who presented to the hospital with diffuse abdominal pain, nausea,
vomiting, watery diarrhea, and subjective fevers for 2 days. On physical exam, she was dehydrated with 102.7° fever.
She had abdominal distension with hepatomegaly and was diffusely tender to palpation with voluntary guarding. Her
liver function tests were unremarkable, and stool studies were normal. She continued to have fevers and her
abdominal symptoms worsened. A bedside diagnostic paracentesis was performed and ascitic fluid analysis revealed
spontaneous bacterial peritonitis requiring IV antibiotics. CT Abdomen/Pelvis was suggestive of Budd-Chiari
Syndrome, and CT Triple Phase confirmed the diagnosis.
Discussion
Subacute Budd-Chiari Syndrome should be considered in patients who have an insidious onset of unexplained liver
dysfunction. Our patient had many factors that contributed to her diagnosis: an extensive rheumatologic history, failed
pregnancies, prolonged hospital stay, and antiphospholipid antibody syndrome. Studies have shown that medical
management is effective for patients who present subacutely. It is not surprising her symptoms resolved with
anticoagulation.
Conclusions
Subacute Budd-Chiari Syndrome is an uncommon clinical condition that must be addressed in a timely fashion to
prevent propagation of a thrombus and potential damage to the liver. Furthermore, it is imperative to evaluate all
prothrombotic conditions while investigating the etiology of Budd-Chiari Syndrome to gain a better understanding of
the cause. If this workup is performed efficiently, the likelihood of a patient requiring a liver transplant is minimal.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Nina Ahuja : ACG Non-Member
Peter Ricketti : ACG Non-Member
Ned O'Karter : ACG Non-Member
Ketherine Kim : ACG Member
Arun Samanta : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1743762
TITLE: The Vanishing Liver Mets
PRESENTER: Bryan O'Connell
PRESENTER (INSTITUTION ONLY): Summa Akron City Hospital
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction: Clinicians have become increasingly reliant on imaging studies to make diagnoses. Despite
improved sensitivity of these imaging modalities some diagnoses cannot be made without biopsy. We present a case
of pylephlebitis in which the radiographic evidence pointed overwhelmingly to metastatic disease. To our knowledge
this is the first reported case of pylephlebitis mimicking colon cancer with liver metastases.
Case: A 65 year old female with a history of hypertension and hypothyroidism presented with six weeks of fatigue,
weight loss, fever and jaundice. She had a laparoscopic cholecystectomy three years ago for cholelithiasis. Initial
workup revealed leukocytosis with bandemia (WBC 20,200, 17 % bands), elevated bilirubin (7.4 mg/dl) and liver
enzymes with an obstructive pattern (alkaline phosphatase 503 U/L, AST 82 U/L, ALT 96 U/L). Blood and urine
cultures were obtained and ertapenem was begun empirically. Abdominal CT with oral and intravenous contrast
showed portal vein thrombosis, multiple liver lesions consistent with metastases, and an ascending colon stricture,
leading to extensive oncologic and gastroenterological evaluation. No intrahepatic or extrahepatic biliary dilation or
stricture was seen on MRCP, but it showed numerous hepatic masses concerning for metastases. Liver biopsy
showed biliary obstruction but no neoplasm. She remained febrile despite negative blood and urine cultures. After
expanding antibiotic coverage to piperacillin/tazobactam and azithromycin she improved clinically and her bilirubin and
transaminases decreased. Colonoscopy showed diverticulosis without masses or strictures. She was diagnosed with
pylephlebitis and discharged home on amoxicillin/clavulanate and anticoagulation. One month later she was
asymptomatic, her jaundice had resolved, and repeat abdominal CT showed a patent portal vein and complete
resolution of the hepatic lesions.
Conclusion: Pylephlebitis is a rare disorder that carries a high morbidity and mortality despite early detection with CT
imaging and broad spectrum antibiotics. Greater than 80% of documented cases contain an identifiable infectious or
inflammatory etiology. Our patient lacked demonstrable intra-abdominal, urinary and blood-borne infection, but rather
had radiographic findings that strongly suggested colon cancer with liver metastases. Multiple lesions in the liver are
often malignant, but clinicians should keep their differentials open to other etiologies. Pylephlebitis should be
considered in a patient with fever, abnormal liver function tests, and portal vein thrombosis.
Methods: n/a
Results: n/a
Conclusion: n/a
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: Yes
Extra Info: : All of the above questions should be not applicable.
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Bryan O'Connell : ACG Non-Member
Rex Wilford : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3.67
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1743769
TITLE: Drug-induced liver injury associated with the glucagon-like peptide 1 (GLP-1) agonist liraglutide
PRESENTER: Emily Kern
PRESENTER (INSTITUTION ONLY): Northwestern University
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Data on the adverse event profiles of the incretin-based hypoglycemic agents are limited. We present the
first case of drug-induced liver injury (DILI) secondary to the glucagon-like peptide 1 (GLP-1) agonist liraglutide.
Case: A 29-year-old woman with type 2 diabetes and vitiligo presented with 10 days of nausea, emesis and acute
hepatitis. Other than starting liraglutide 1.2mg daily four months prior, the patient reported no medication changes,
supplements or acetaminophen use. Her social history was unremarkable. Admission labs: AST 991 U/L, ALT 1123
U/L, bilirubin (total/direct) 9.5/6.2 mg/dL, alkaline phosphatase 90 U/L, platelets 224 K/uL, and INR 1.3. Physical exam
revealed a nontender abdomen and intact mentation. Liver ultrasound showed increased periportal echogenicity and
no biliary dilation. Extensive evaluation for viral (A-E, CMV, EBV, adenovirus), autoimmune and metabolic causes was
unrevealing. Liver biopsy showed acute hepatitis with mixed infiltrate, significant eosinophils, rare plasma cells and no
interface hepatitis (Figure 1a-b). The patient was discharged, but nine days later developed worsening symptoms and
rising transaminases. She was admitted for repeat biopsy, which showed hepatic necrosis and an extensive
eosinophilic infiltrate (Figure 1c-d). Steroids were started for presumed marker negative drug induced autoimmune
hepatitis and continued given clinical improvement. Six months after stopping liraglutide, AST/ALT are 143/156 U/L,
total bilirubin is 3.0 mg/dL, and INR is 1.0.
Discussion: This is the first reported case of liraglutide-induced hepatitis. Liraglutide is an incretin-based drug, along
with the dipeptidyl peptidase-4 (DPP-4) inhibitors that have been implicated in cases of DILI. Initial GLP-1 studies did
not report hepatotoxicity, although they were likely underpowered. Hepatotoxicity may be an incretin analogue class
effect with a long latency period. Post-marketing studies are needed to define the hepatotoxic potential of GLP-1
agonists.
Methods: n/a
Results: n/a
Conclusion: n/a
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Emily Kern : ACG Non-Member
Lisa VanWagner : ACG Member
Mary Rinella : ACG Member
Figure 1: Liver Histology, hematoxylin & eosin stain: A. Infiltration of a portal tract with predominantly eosinophils B.
High power view demonstrating ballooning change and eosinophilic infiltrate C. Submassive hepatic necrosis D. High
power view of adjacent preserved liver with eosinophilic infiltrate
IMAGE CAPTION: Figure 1: Liver Histology, hematoxylin & eosin stain: A. Infiltration of a portal tract with
predominantly eosinophils B. High power view demonstrating ballooning change and eosinophilic infiltrate C.
Submassive hepatic necrosis D. High power view of adjacent preserved liver with eosinophilic infiltrate
(no table selected)
AVERAGE SCORE: 3.33
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1743796
TITLE: An Unusual Cause of Hepatic Dysfunction and Ascites After Lumbar Spine Surgery
PRESENTER: Renuka Jain
PRESENTER (INSTITUTION ONLY): Rocky Mountain Clinical Research
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Extrahepatic causes of passive congestion are often attributed to conditions involving the hepatic vein or due
to right heart dysfunction. We present a case of liver disease, resulting in hepatic dysfunction and ascites, originating
from an unusual source. A 37 yo male presented with a two-month history of abdominal discomfort, bloating, and
dyspnea. He reports a CT scan of the abdomen, which described ascites and small pleural effusions. One year prior,
he was diagnosed with non-alcoholic steatohepatitis due to hyperlipidemia. His baseline liver function tests (LFT's)
showed an ALT 87 U/L, AST 39 U/L, Alkaline Phosphatase (AP) 28 U/L, total bilirubin (TB) 0.5 mg/dL, and albumin
4.8 g/dL. He now complained of increasing abdominal girth and fatigue. PE was significant for a loud systolic murmur
at the right sternal border radiating to the back and over the entire abdomen along with peripheral edema. LFT's
showed an ALT 86 U/L, AST 68 U/L, AP 57 U/L, TB 1.7 mg/dL, albumin 4.1 g/dL, with BUN 14 mg/dL, Creatinine 1.1
mg/dL, and a normal CBC. Ultrasound (US) with Doppler showed mild ascites and normal portal and hepatic venous
flows. A bubble ECHO was normal. We reviewed the prior CT scan and found a possible fistulous connection from the
left iliac artery to the iliac vein. Doppler US revealed pulsatile venous flow in the left iliac venous system, consistent
with an arteriovenous fistula. A CT angiogram revealed that the IVC was isodense with the abdominal aorta,
opacification of the left internal and external iliac arteries but none in the right iliacs, and enlargement of the left iliac
vein. The right atrium was enlarged with contrast flowing in a retrograde fashion into the hepatic vein, suggesting right
heart failure. The diagnosis of a left iliac artery to iliac vein fistula was made. He then underwent placement of a
coated stent in the iliac artery across the fistula. Two months later he noted dramatic improvement in energy levels,
absence of fatigue and ascites, and no dyspnea. LFT's showed ALT 99 U/L, AST 56 U/L, AP 47 U/L, TB 0.7 mg/dL,
and albumin 4.2 g/dL, similar to his baseline levels. The AV fistula lead to right heart failure with resultant passive
congestion of the liver and development of ascites and abnormal liver function tests. Additional history revealed that
he had undergone L4/L5 disk surgery five months prior to presentation. Our conclusion is that instrumentation during
this surgery lead to inadvertent trauma to the iliac artery, leading to the development of the fistula. This unusual case
of passive congestion demonstrates the value of a complete history and physical to consider more remote causes of
right heart failure resulting in hepatic dysfunction and ascites.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Renuka Jain : ACG Non-Member
Rajesh Jain : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1743814
TITLE: An unusual case of rapidly progressive hepatic failure and death due to primary hepatic AL (kappa)
amyloidosis.
PRESENTER: Manan Pandya
PRESENTER (INSTITUTION ONLY): UMDNJ-NJMS
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Hepatic amyloidosis is a rare infiltrative disease involving the liver. Although hepatic involvement is common
in systemic amyloidosis, clinically significant liver failure is very rare. This is an unusual case of a 62 y/o man with past
medical history of DM Type II, HTN, and Chronic renal insufficiency who initially presented with symptoms of weight
gain, abdominal distension, altered mental status, worsening fatigue and diarrhea over a period of 3 weeks. He was
found to have hepatomegaly and ascites on exam, while lab studies showed evidence of acute renal failure, severe
anemia and coagulopathy. An ultrasound of the abdomen showed evidence of ascites and hepatosplenomegaly, while
EGD showed evidence of small esophageal varices and portal hypertensive gastropathy. A biopsy of the liver was
performed for further evaluation, which showed atrophic hepatocytes with severe sinusoidal deposition of
homogenous eosinophilic material with a positive congo-red stain showing apple green birefringence consistent with
amyloid deposits. The sample was further sent for liquid chromatography tandem mass spectrometry which detected
a peptide profile consistent with AL (kappa) amyloid deposition. His hospital course became complicated with oral and
gastric mucosal bleeding refractory to replacement of coagulation factors. Also, complications of dialysis dependent
renal failure, hypoxic respiratory failure, and gram negative sepsis further contributed to his declining condition. He
died soon after from hypovolemic shock secondary to ongoing mucosal bleeding refractory to treatment. Patients with
primary systemic amyloidosis who have biopsy-proven liver involvement (primary hepatic amyloidosis) have a poor
prognosis; the median survival of patients has been reported as 8.5 months, while in this case he rapidly deteriorated
within 6 weeks of being diagnosed for amyloidosis.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Manan Pandya : ACG Non-Member
Suman Manchireddy : ACG Non-Member
Pavan Patel : ACG Non-Member
Ravishankar Ramamoorthy : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.33
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1743950
TITLE: A Rare Case of Multiple Myeloma with Nodular Liver Lesions
PRESENTER: Mark Postacchini
PRESENTER (INSTITUTION ONLY): Department of Internal Medicine, Advocate Lutheran General Hospital
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A fifty eight year old male with chronic obstructive pulmonary disease presented with acute left rib pain. An
X-ray revealed a rib lesion which was biopsied. Histopathology was consistent with a plasmocytoma. Further
diagnostic workup and a skeletal survey revealed multiple myeloma (MM). The patient was treated with chemotherapy
and an autologous stem cell transplant resulting in a complete remission. 15 months later, the abdominal pain
recurred and CT scanning of the abdomen revealed multiple liver lesions. Biopsy was consistent with MM. The
patient was treated with chemotherapy and a second autologous stem cell transplant. Eight months later, the patient
presented with recurrent abdominal pain and testing revealed rapid progression of MM. An experimental trial of
chemotherapy resulted in a clinical remission. Two months later, recurrent abdominal pain and laboratory testing
revealed acute hepatic failure and the patient expired.
Plasma cell myeloma can present as a solitary plasmacytoma or with multiple lesions. Within the bone marrow,
myeloma cells replicate and disseminate systemically causing extra-nodal disease. Current MM staging systems: the
International Staging System and the Durie-Salmon Staging System utilize various laboratory tests for staging and
prognostication. However, the two systems and the National Comprehensive Cancer Network only recommend
skeletal survey imaging. It is unknown if the patient had liver involvement at the time of presentation or not which
could have changed treatment and prognosis. To the best of our knowledge, multiple myeloma with nodular liver
lesions is extremely rare and there have only been 27 cases reported. One study concluded MM with gastrointestinal
involvement occurs in only 0.9% of MM cases. Gastrointestinal involvement has a rapid post stem cell transplant
relapse rate and an overall worse prognosis. This case reminds clinicians to include multiple myeloma in the
differential diagnosis of liver lesions. This case also highlights the potential benefit to using advanced imaging in the
initial diagnostic evaluation of MM to more precisely stage and prognosticate.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Mark Postacchini : ACG Non-Member
Izabela Postacchini : ACG Non-Member
Leonard Klein : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 2.67
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1743967
TITLE: An unusual cause of Jaundice: Cholestasis-lymphedema syndrome
“ Aagenaes syndrome”
PRESENTER: Meer Ali
PRESENTER (INSTITUTION ONLY): University Hospitals Case Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 61-year-old Caucasian male of Norwegian descent presented to the emergency department with
complaints of progressive jaundice, pruritus, dark urine, clay colored stools and lower extremity edema for 1 month.
This patient had history of intermittent jaundice all of his life with chronic lower extremity edema. As an infant he had
an exploratory laparotomy for biliary atresia (but no definitive intervention was done). There was no family history of
liver disease, no history of alcohol use and his only medication was furosemide. On examination he had no stigmata
of chronic liver disease, reduced air entry in both lower lung fields, a healed laparotomy scar and 2 + bilateral pedal
edema. Initial labs showed a normal complete blood count and renal function but a total bilirubin of 6.7 (Direct 4.2),
alkaline phosphatase of 422 with AST 41 and ALT 32. A chest X-ray done in the ED revealed bilateral pleural
effusions. Subsequent work up for chronic liver disease was negative and liver ultrasound with dopplers and MRI of
the liver were negative. A liver biopsy showed chronic lymphocytosis. Thoracentesis demonstrated chylothorax with
triglycerides of 815 mg/dl. In summary, this is a 61 y/o Caucasian male of Norwegian heritage with recurrent,
intermittent, cholestatic jaundice with chronic lymphedema, pruritus and chylothorax. Given this constellation of
findings,we diagnosed our patient with Aagenaes syndrome. This syndrome was first described in 6 large Norwegian
families and is characterized by chronic lymphedema and cholestasis. Its inheritance is autosomal recessive with a
prevalence of < 1 in 100,000. Pathogenesis involves a defect in lymphangiogenesis with generalized hypoplasia of
lymphatics and the abnormal development of lymphatics around small biliary tracts. Patients present with severe
neonatal cholestasis, which decreases during early childhood and becomes episodic later. Lymphedema is present at
birth, but is usually noticed later, and affects the small bowel and thoracic soft tissue leading to chylothorax. Liver
histology may show non-specific inflammation (as in our patient), giant cell transformation, fibrosis or cirrhosis.
Prognosis for liver disease is good. Management involves eating a fat reduced diet during cholestasis with
supplementation of fat-soluble vitamins. We used subcutaneous Octreotide for the chylothorax with resolution of his
pleural effusions. The patient is doing well currently and is being followed in the hepatology clinic.
Methods: NA
Results: NA
Conclusion: NA
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Meer Ali : ACG Member
Caroline Soyka : ACG Non-Member
Wajeeh Salah : ACG Member
Marina Silveira : ACG Member
Yngve Falck-Ytter : ACG Member
Anthony Post : ACG Non-Member
Ashley Faulx : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 1.67
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1743988
TITLE: Hepatopulmonary Syndrome (HPS): A missed diagnosis
PRESENTER: Rushikesh Shah
PRESENTER (INSTITUTION ONLY): SUNY upstate medical university
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: The diagnosis of HPS is often missed due to lack of suspicion. Patients with a diagnosis of HPS can be
allocated extra points on the liver transplant wait list to enhance the possibility of receiving an allograft within 3
months. We present a case where the diagnostic work up revealed completely unsuspected HPS in a patient with
decompensated cirrhosis.
A 64 year old male patient with a known history of COPD and liver cirrhosis secondary to non-alcoholic steatohepatitis
(NASH) presented for evaluation of worsening ascites. He had a 6 weeks history of worsening dyspnea while on 2L of
oxygen at home. Physical examination revealed hypotension 100/64 and tachypnea. The oxygen saturation was 86%
in the standing position and 89% when supine position. He had reduced air entry at the right lung base and a
moderately distended abdomen. Chest x-ray showed right sided pleural effusion. Both paracentasis and
thoracocentasis revealed ascites due to portal hypertension and hepatic hydrothorax. Despite improvement in the
chest x-ray for next 2 days, the patient remained dyspneic with increased oxygen requirements. As the patient’s
pulmonary function tests (PFT) were essentially unchanged from PFTs done three years prior, we considered
uncommon underlying pathology. Arterial blood gases in the sitting position showed primary respiratory alkalosis with
arterial oxygen (PO2) of 57.8 mm Hg and A-a gradient of 60.05. HPS was suspected and echo bubble study revealed
a delayed right to left intrapulmonary shunt. The diagnostic criteria for HPS were fulfilled. This case was classified as
severe HPS, based on the PaO2. The patient was discharged home with an increase in oxygen to 4 L and is currently
being evaluated for liver transplant. HPS is an entity affecting the pulmonary vascular morphology in chronic liver
disease patients characterized by a defect in arterial oxygenation. The presentation of HPS can be atypical or masked
with co-existing lung diseases. The five year survival rate in patients with HPS is 23%, compared to 63% in those
without HPS and with similar MELD scores. It is imperative to have a high index of suspicion for HPS in a patient
presenting with liver disease and hypoxia. This progressive phenomenon with ominous prognosis has become an
indication for urgent liver transplantation. This is because complete resolution of HPS in most cases occurs after liver
transplant. Awareness among healthcare providers and early diagnosis are crucial.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Rushikesh Shah : ACG Non-Member
Omar Mousa : ACG Non-Member
Aakash Aggarwal : ACG Non-Member
Divey Manocha : ACG Non-Member
Savio John : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3.67
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1743999
TITLE: Chronic Transaminitis: When It’s Not the Liver
PRESENTER: Nicole Gentile
PRESENTER (INSTITUTION ONLY): Mayo Clinic
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 40 year old male with history of chronically elevated liver transaminases presented to the emergency
department with dyspnea. He was diagnosed with a pulmonary embolism and admitted with hypercapnic respiratory
failure.
His past medical history is significant for chronic transaminase elevation since the age of 9. A thorough evaluation in
the past including abdominal ultrasounds, CT scans, ERCP, two liver biopsies at age 17 and 25, both unremarkable,
hepatitis serologies, alpha one anti-trypsin level, and investigations for autoimmune disease were all unrevealing.
He has a long standing history of intermittent abdominal pain lasting minutes at a time up to several times a month. He
has had episodes of alternating nonbloody diarrhea and constipation in the past. Colonoscopy and EGD at age 39
were unremarkable except mild erosive antral gastritis with no evidence of helicobacter pylori or celiac disease. He is
a current smoker smoking 5 cigarettes per day for the past 20 years, but does not drink alcohol or use illicit drugs.
Family history is significant for a younger sister with asymptomatic liver enzyme elevation. He was given a tentative
diagnosis of autoimmune hepatitis. He lost 20 to 30 pounds unintentionally over 1.5 years. In the six months prior to
presentation he described significant muscular weakness to the extent of having difficulty getting out of bed.
During hospitalization here, initial evaluation demonstrated immunity to hepatitis B, negative hepatitis C serology, as
well as negative ceruloplasmin level, antibodies to Liver Kidney Microsome 1, ICAM, anti-smooth muscle antibody,
ANA, SS-A Ro IgG, SS-A La IgG, smith antibody, RNP antibody, Scl 70 antibody, Jo1 IgG antibody, cyclic citrullinated
peptide antibodies, striated muscle antibody. AST was 71 (8-48 U/L), ALT 71 (7-55 U/L), total bilirubin 0.1 (0.1-1.0
mg/dL), ammonia 65 (<50 mcg N/dL), G-glutamyltransferase 12 (8-35 U/L). Creatinine kinase was elevated at 732
(52-336 U/L).
He underwent a muscle biopsy demonstrating vacuoles filled with Periodic Acid Schiff stain positive material
consistent with alpha glucosidase deficiency/glycogen storage disease type II. Full gene sequencing detected a
heterozygous sequence c.-32-13T>G, which is associated with a deleterious mutation in late onset Pompe disease.
Therefore, our patient, who presented with chronically elevated transaminases was diagnosed with Pompe disease, a
rare autosomal recessive disease, and was initiated on treatment with enzyme replacement. His sister will undergo
evaluation up per suggestions from medical genetics. Thus, in a patient with chronically elevated transaminases and
muscular weakness, one should consider Pompe disease in the differential.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Nicole Gentile : ACG Non-Member
Sahil Khanna : ACG Member
Vandana Nehra : ACG Member
Konstantinos Lazaridis : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 2
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1744017
TITLE: Calciphylaxis in a Patient with Alcoholic Cirrhosis
PRESENTER: Ehsaan Akhtar
PRESENTER (INSTITUTION ONLY): UC Davis Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose:
Background: Calciphylaxis is a rare syndrome characterized by cutaneous ischemic necrosis secondary to vascular
calcification. The condition is almost exclusively seen in end-stage renal disease (ESRD), but has also been
associated with cirrhosis in seven case reports. The pathogenesis is unknown but commonly described risk factors
include female sex, Protein C and S deficiency, and high calcium-phosphorus product.
Objective: Here we report a case of calciphylaxis in a cirrhotic patient with normal kidney function. We also provide a
review of the existing literature.
Case Presentation: A 38 year old woman with alcoholic cirrhosis who was directly admitted with a recurrent lower
extremity rash. The patient initially presented one year prior with abdominal pain, fatigue, and a violaceous rash over
the abdomen and proximal lower extremities, biopsy of which demonstrated calciphylaxis. At that time she improved
with local wound care and sodium thiosulfate therapy, but was readmitted with recurrence of a painful lower extremity
rash. On exam there was evidence of a healed skin graft on her left thigh with surrounding punctate erythema that
was tender to palpation. Her abdomen was soft and nondistended, with hepatosplenomegaly. Lab values were
significant for Ca-Phos product of 39, normal protein C and S levels, normal PTH, BUN 13 mg/dl and creatinine 0.42
mg/dl. Connective tissue disease screens and malignancy screens were negative. She had not been receiving
albumin infusions or blood transfusions. The patient responded well to sodium thiosulfate therapy and local wound
care although her rash remained. She was discharged with a plan to continue 2 months of sodium thiosulfate therapy
as an outpatient.
Conclusions: Here we describe the phenomenon of calciphylaxis in the background of alcoholic cirrhosis. Our patient
is notable in comparison to previous case report patients for having normal protein C and S levels, a low calciumphosphorus product, and normal serum creatinine. Further studies are necessary to uncover potential sensitizing
factors for the development of calciphylaxis in non-ESRD patients, specifically those with alcoholic cirrhosis.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Ehsaan Akhtar : ACG Non-Member
Dhavan Parikh : ACG Non-Member
Natalie Torok : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 2.67
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1744055
TITLE: Intrahepatic Biliary Strictures mimicking sclerosing cholangitis in Hepatic Sarcoidosis
PRESENTER: Samyuktha Ramavaram
PRESENTER (INSTITUTION ONLY): University or Arkansas for Medical sciences
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction:
Hepatic Sarcoidosis can have varied clinical features and presentations, of which a rare one is intrahepatic biliary
strictures resembling primary sclerosing cholangitis (PSC). We report a case of Hepatic Sarcoidosis where imaging
showed multiple strictures of intrahepatic ducts resembling PSC and Liver biopsy revealed noncaseating granulomas
suggestive of Sarcoidosis.
Case Presentation:
A 27 year old woman with morbid obesity was admitted with four month history of weight loss of 60 lbs, epigastric pain
and intermittent jaundice. Labs revealed Total Bilirubin of 5.5, Direct Bilirubin of 4.6, AST of 192, ALT of 65 and
Alkaline Phosphatase of 1197. Hepatitis Screen was negative. MRCP showed multiple strictures of intrahepatic ducts
with some mild focal dilatation, suggestive of sclerosing cholangitis. No extrahepatic duct dilatation or stones were
seen in biliary tree. Hepatosplenomegaly and multiple hypointense lesions in spleen were seen suggestive of
lymphoma or granulomatous involvement. Enlarged lymph nodes (LN's) measuring 2 cm were seen in
retroperitoneum and portocaval region. Biopsy of the retroperitoneal LN's showed non-caseating granulomas.
Subsequently liver biopsy was performed which showed noncaseating granulomas, lymphocytic cholangitis, bile duct
epithelial damage, and chronic cholestasis. ACE level was 123 U/L. Pt was discharged on ciprofloxacin and
prednisone.
Discussion:
Hepatic involvement is seen in 95% of patients with sarcoidosis. Histology shows multiple, diffuse non-caseating
hepatic granulomas. Clinical features may include nausea, vomiting, jaundice, abdominal pain and
hepatosplenomegaly. Minority of cases can be severe and rapidly progressive, leading to cirrhosis, portal
hypertension, chronic cholestasis and Budd-Chiari syndrome.
The treatment of sarcoidosis with hepatic involvement remains controversial. The most widely accepted treatment
involves use of glucocorticoids in patients with symptomatic sarcoidosis and evidence of cholestasis or elevated liver
transaminases. The use of glucocorticoids does not alter the course and progression of the disease. Splenectomy is
another option in patients with portal hypertension, symptomatic splenomegaly and severe hypersplenism. In
advanced Hepatic Sarcoidosis, transplantation is the only option considered curative.
Conclusion:
Hepatic Sarcoidosis is a rare clinical entity with a wide spectrum of clinical presentations and variable progression.
Diagnosis is made by clinical and radiologic findings suggestive of sarcoidosis, along with histopathologic findings of
non-caseating granulomas on liver biopsy, after the exclusion of other causes of hepatic granuloma formation.
Treatment remains controversial.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Samyuktha Ramavaram : ACG Non-Member
Mohit Girotra : ACG Member
Neelima Velchala : ACG Member
Suman Siddamreddy : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1744110
TITLE: Primary Hepatic Lymphoma in an African American Male: A case report.
PRESENTER: Cortni Tyson
PRESENTER (INSTITUTION ONLY): Howard University Hospital
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Purpose: To highlight a case of Primary Hepatic Lymphoma presenting in an African American Male.
Methods: Methods: The study design is a retrospective chart review. The study subject was identified through the
pathology department via histologic evaluation from biopsy data consistent with primary hepatic lymphoma. Exclusion
criteria included patients with other hepatic lesions, including metastatic disease, Hepatocellular carcinoma or hepatic
hemangioma.
Results: Case: A 45-year-old African American male with a history of hepatitis-C presented with complaints of left
upper quadrant pain, fatigue, purities, 15 lbs weight loss and night sweats for 3 months. Physical examination was
significant for icteric sclera, jaundice and non tender hepatomegaly. Laboratory investigation showed normal
electrolytes, total bilirubin of 6.1, AST 150, ALT 142, alk phos 282 and AFP of 2. Hepatitis serologies were negative.
CT showed multiple masses in right lobe of liver with the largest mass measuring 8.1 x 6.7 x 8.8 cm. EGD and
colonoscopy were negative for malignancy, and a liver biopsy showed diffuse infiltration by lymphoid cells with focal
areas of necrosis, with immunohistochemistry positive for CD20, CD10 & bcl6. Thus a diagnosis of primary diffuse
large B cell lymphoma was made. During his hospital course his total bilirubin increased to 23 and patient received
adjuvant radiation therapy to relieve his biliary. Subsequently his bilirubin improved facilitating initiation of R-CHOP
chemotherapy, to which the patient responded. He is still currently undergoing chemotherapy at our institution.
Conclusion: Discussion: Primary hepatic lymphoma is a rare disease that accounts for less than 1% of primary liver
tumors [2]. Published case reports have focused on Japanese and Chinese patients [1,4,5,10], but very few include
African American patients. Areas of the world are known for higher incidences of both Hepatitis B virus and for
Hepatitis C virus and lymphoma has been associated with chronic long-standing liver disease of many etiologies
[1,4,5,9]. Patients with lymphoma in the liver, primary or extranodal in origin, will present with constitutional
symptoms. It is important to be aware of this rare tumor being associated with minority patients. The literature has
shown the efficacy of CHOP chemotherapy for such lesions [3, 12, 19], and our patient has responded well to this
therapy to this date. This case demonstrates a rare primary tumor not previously associated with the African American
population. As more patients present with chronic liver disease, it will be important to recognize this rare but treatable
disease within the African American community.
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Cortni Tyson : ACG Member
Sri Lakshmi Yeruva : ACG Non-Member
Rehana Begum : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3.67
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1744112
TITLE: Tension hepatic hydrothorax in a cirrhotic patient
PRESENTER: Habeeb Salameh
PRESENTER (INSTITUTION ONLY): University of Texas Medical Branch. Department of Internal Medicine
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 61 year old male with past medical history of HCV/alcoholic cirrhosis presented to the emergency room
with large volume hematemesis. He had normal vital signs. Labs revealed anemia (8.9 g/dl), thrombocytopenia
(92/micl), prolonged prothrombin time/INR (17.9 sec/1.5), and low albumin (1.8 g/dl). Emergent EGD showed large
esophageal varices with red whale sign, Mallory-Weiss tear, gastric varices, and cardiac ulcer -visible vessel and
oozing blood-. The oozing ulcer was treated with epinephrine injection and clip hemostasis. Six esophageal bands
were placed. CT abdomen showed minimal ascites and mild right sided pleural effusion. Following another episode of
hematemesis he became hemodynamically unstable and required aggressive resuscitation with intravenous fluids,
packed RBCs, and cryoprecipitate. Afterwards he had no further overt GI bleeding with improvement in his vital signs
but six hours later he had tachypnea, tachycardia, and hypoxia requiring high flow oxygen (50% oxygen, 10 L/min).
Chest X-ray showed a tension right sided hydrothorax and arterial blood gas revealed acute hypoxic respiratory
failure. Thoracentesis drained 2.1 L of transudative fluids and his vitals improved. CT thorax showed hydrothorax,
minimal ascites and no pericardial effusion. He was restarted on spironolactone and furosemide with significant
reduction in his hydrothorax. In the setting of gastric varices, esophageal varices, significant upper gastrointestinal
bleeding, and hepatic hydrothorax he was offered evaluation for TIPS but refused and was discharged on diuretics.
Hepatic hydrothorax develops due to the passage of ascitic fluid from the peritoneal cavity to the pleural space
through diaphragmatic defects. This is driven by the hydrostatic gradient of negative intrathoracic pressure along with
the positive intraabdominal pressure producing a unidirectional flow of ascitic fluid into the pleural space. We believe
that clinicians should be aware of the possibility of developing tension hepatic hydrothorax following aggressive
resuscitation with IV fluids and blood products in cirrhotic patients especially if it is associated with severe
hypoalbuminemia.
Methods: NA
Results: NA
Conclusion: NA
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Habeeb Salameh : ACG Member
Scott Larson : ACG Member
Ragai Meena : ACG Non-Member
Alexander Duarte : ACG Non-Member
Roger Soloway : ACG Non-Member
IMAGE CAPTION:
(no table selected)
AVERAGE SCORE: 4.67
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1744120
TITLE: Hepatomegaly Evaluated Intra-operatively at Bariatric Surgery
PRESENTER: Ekta Gupta
PRESENTER (INSTITUTION ONLY): Washington Hospital Center/ Georgetown University
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction
Hepatomegaly is a common finding in patients undergoing bariatric surgery. Steatosis is the usual cause of
hepatomegaly in this population with 33% of morbidly obese patients showing fatty infiltration of majority of their
hepatocytes. Here we present an interesting patient where planned bariatric procedure had to be aborted due to
laparoscopic finding of a mesenteric mass which was the perceived to be hepatomegaly on pre-operative clinical
examination.
Case Report
A 44 year old morbidly obese female with body mass index of 54 was referred for gastric banding. Preoperative
examination and workup including esophagogastrodeudonoscopy (EGD) was unremarkable other than presence of
palpable liver a few centimeters below the costal margin. This finding was again identified just before making incision
prior to laparoscopy with the plan to perform gastric banding. Diagnostic laparoscopy however showed presence of a
12x15 cm mesenteric mass at the right side of the root of the mesentery. This mass was the cause of perceived
hepatomegaly pre-operatively as the size of the liver on laparoscopy was normal. The planned bariatric procedure
was aborted. Interestingly, subsequent CT scan of the abdomen which was done to better characterize the mass,
confirmed normal liver size but failed to identify any discrete mass. MRI was able to characterize the mass and
subsequently patient underwent surgical excision of the mass. Histo-pathology revealed a well differentiated/low grade
liposarcoma.
Discussion
This case demonstrates atypical asymptomatic presentation of mesenteric liposarcoma with right upper quadrant
mass which was perceived as hepatomegaly. Even though hepatomegaly is common in obese patients, and American
Association for the Study of Liver Diseases (AASLD) guidelines recommend to not screen obese patients for liver
disease, this case shows that presence of right upper quadrant mass on examination may not always represent
hepatomegaly and additional workup may be needed pre-operatively. In our patient, the liposarcoma was interestingly
not even identified on CT scan and hence, patient with high clinical suspicion should have additional imaging like MRI.
Pre-operative recognition of this could have avoided surprises during laparoscopy that led to abortion of the
procedure.
Conclusion
This case highlights the importance of comprehensive clinical examination prior to bariatric surgery especially in
morbidly obese patients where this may be difficult to perform. Enhanced awareness among bariatric
gastroenterologists of this atypical presentation of mesenteric liposarcoma can help in its pre-operative recognition
which can avoid unanticipated challenges during the bariatric surgery.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: Yes
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Ekta Gupta : ACG Member
Farzin Rashti : ACG Member
Won Cho : ACG Member
Timothy Shope : ACG Non-Member
Timothy Koch : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.33
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1744138
TITLE: An Unusual Presentation of Lymphoma in the Liver: A case report of a Female of African descent.
PRESENTER: Cortni Tyson
PRESENTER (INSTITUTION ONLY): Howard University Hospital
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: To present an unusual presentation of lymphoma in the liver in an African American Female.
Methods: The study design is a retrospective chart review. The study subject was identified through the pathology
department via histologic evaluation from biopsy data consistent with lymphoma in the liver. Exclusion criteria included
patients with other hepatic lesions, including metastatic disease, Hepatocellular carcinoma and hepatic benign lesions.
Results: A 54 year old female from Guyana presented with hematemesis of one day duration. On exam her vital signs
were stable, she was anicteric, and had no conjunctival pallor. Further investigations noted a hemoglobin of 8.5mg.
Other lab investigations were normal, including negative hepatitis serologies. EGD showed a large ulcerated friable
10cm mass in the proximal body of the stomach. CT scan showed two small lesions in the left lobe of the liver 2.5cm
in diameter. Biopsy results from the gastric mass and liver lesions confirmed stage IV large high grade b-cell
lymphoma with cells positive for CD20, CD79A, CD10, and BCL6 and negative for H-pylori. The patient underwent RCHOP therapy with little response after 7 cycles. Nine months later, the patient presented with jaundice, hypotension,
fever, and dark colored emesis. Total bilirubin was elevated at 9.8, AST was 94, ALT 78, Alkaline phos 192,
Hemoglobin 8.9mg. Repeat CT scan showed large necrotic mass in the left lobe of the liver, involving the stomach,
encasing numerous structures, including the common bile duct. Palliative biliary stent was placed, and the patient had
several sessions of palliative radiation therapy.
Conclusion: Hepatic involvement of lymphoma is not uncommon, accounting for about 30- 40% of all patients with
lymphoma [11]. There have been many published case reports in Japanese patients and Chinese patients [1,4,5,10],
but very few case reports have included patients of African American descent. The majority of patients with lymphoma
in the liver, primary or extranodal in origin, will present with some constitutional symptoms, however, our patient
presented with upper gastrointestinal bleed. Current literature has noted good response to these aggressive
lymphoma lesions in the liver and GI tract [3,14,19,23] with(R) CHOP widely known as first line treatment [21,22,19].
There continue to be efforts made to investigate new treatment strategies for late stage disease as well as
chemotherapy non-responders, such as in our patient. Unfortunately, our patient was not eligible for any current
clinical trials, and was lost to follow up.
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Cortni Tyson : ACG Member
Sri Lakshmi Yeruva : ACG Non-Member
Rehana Begum : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1744142
TITLE: An Interesting Case of Recurrent Gastrointestinal Bleed due to Gastric Varices Successfully Treated with
Balloon-occluded Retrograde Transvenous Obliteration (BRTO)
PRESENTER: Ekta Gupta
PRESENTER (INSTITUTION ONLY): Washington Hospital Center/ Georgetown University
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction
Balloon-occluded Retrograde Transvenous Obliteration (BRTO) to treat gastric varices was first described in Japan in
1996, however, it is rarely used in United States (US). BRTO is not even mentioned in US (American Association for
the Study of Liver Diseases - AASLD) guidelines on treatment of variceal hemorrhage. Here we present an interesting
case of gastric varices treated with BRTO.
Case Report
A 64 year old male with known hepatitis C cirrhosis, end stage renal disease, prior hepatic encephalopathy (HE)
presented with recurrent upper gastro-intestinal bleed (GIB) secondary to isolated gastric fundal varices as confirmed
by endoscopy. Due to high MELD score and HE, BRTO was chosen over transjugular intrahepatic portosystemic
shunt (TIPS). Using right groin approach, the splenorenal shunt was catheterized. Venogram identified phrenic vein
draining into the inferior vena cava which was occluded using coil embolization. The splenorenal shunt was then
occluded using a 9 mm balloon and 3% sotradecol was injected into the varices. The occlusion balloon was deflated
after 4 hours. Follow up computed tomography confirmed sclerosis of varices. Patient did not have recurrence of GIB
and was discharged home.
Discussion
An ideal candidate for BRTO is a patient with gastric varices who has factors which increase the risk for TIPS such as
thrombosis of portal vein, high MELD score or encephalopathy as in our patient. BRTO can only be performed if
patent spleno-renal shut is present. It is important to identify the draining outflow veins with systemic communications
and obliterate them if needed to reduce the risk of systemic embolization of the sclerosant as was done in our case.
With appropriate case selection, success rate of 87-100% have been reported with rates of re-bleeding as low as 09%. BRTO does-not cause worsening of hepatic synthetic function or encephalopathy as it increases the portal
perfusion.
Conclusion
BRTO provided safe, effective and durable treatment of gastric varices in our patient. This case report will enhance
awareness of this underutilized procedure so that evidence base data can be generated to establish role and safety of
BRTO in gastric varices.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Ekta Gupta : ACG Member
Jacqueline Laurin : ACG Member
Won Cho : ACG Member
Kirti Shetty : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 2.33
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1744207
TITLE: Seronegative Autoimmune Hepatitis Presenting as Decompensated Cirrhosis
PRESENTER: Daniel Eshtiaghpour
PRESENTER (INSTITUTION ONLY): Harbor UCLA Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose:
A 58 year old Hispanic woman presents one month history of increasing lower
extremity edema, abdominal swelling, lower abdominal pain, and diarrhea. She had
previously experienced a 15 kg weight loss prior to this month and then gained another
10 kg over the past month. Her admission had been prompted as a result of worsening
edema following initiation of diuretic therapy 10 days ago. Examination was significant for
scleral icterus, +3 bilateral lower extremity edema that went up to the thighs, and ascites.
Subsequent studies revealed a nodular liver, impaired synthetic function, a AST:ALT ratio
of 1.3:1 and thrombocytopenia which revealed a diagnosis of cirrhosis.
The patient had no history of alcohol abuse and was taking no hepatotoxic
medications, acetaminophen or herbal supplements. Workup of the etiology of this
cryptogenic cirrhosis revealed a right upper quadrant ultrasound with normal dopplers,
negative hepatitis serologies, normal ceruloplasmin levels, normal Alpha one antitrypsin
levels, and a normal transferrin saturation. In addition, all autoimmune serologies were
negative including ASMA, anti-LKM, ANA, ALC-1 with mildly elevated IgG levels.
Transjugular liver biopsy results were consistent with autoimmune hepatitis. The patient
was started on steroids and azathioprine with normalization of her ALT and AST within
1 month. She is currently on a liver transplant list with a MELD of 10.
Autoimmune hepatitis is a chronic hepatitis that is characterized by immunologic
and autoimmunologic features, generally including the presence of circulating
autoantibodies and high serum globulin concentrations. Type one autoimmune hepatitis is
characterized by circulating antibodies to nuclei (ANA) and/or smooth muscle (ASMA).
Type two autoimmune hepatitis is generally characterized by antibodies to liver/kidney
microsomes (ALKM-1) and/or to a liver cytosol antigen (ALC-1).
The frequency of presumed seronegative autoimmune hepatitis in patients with
acute and acute severe presentations is ≤7%. Patients with acute presentations can have
normal serum γ-globulin levels, centrilobular zone 3 necrosis, and low pre-treatment
international diagnostic scores. Liver tissue examination is essential for the diagnosis, and
hepatic steatosis can be a co-morbid feature. A treatment trial with corticosteroids should
be considered in all patients, regardless of the serological findings, and improvements have
occurred in 67–87% of cases.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Daniel Eshtiaghpour : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3.67
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1744211
TITLE: Acute Hepatitis C: An Unusual Mode of Transmission
PRESENTER: Adeeti Chiplunker
PRESENTER (INSTITUTION ONLY): Medical College of Wisconsin
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction:
Chronic hepatitis C infection is one of the most common causes of chronic liver disease, with evidence of infection in
nearly 4.1 million individuals in the United States. Acute hepatitis C affects about 17,000 people per year. Here, we
present a patient who acquired acute hepatitis C from an unusual mode of transmission.
Case:
Our patient is a 45 year old man who was admitted with nausea/vomiting, jaundice, abdominal pain, acholic stools,
and scleral icterus for the past three months. These symptoms developed approximately two weeks after he debrided
a pustule on his hand with a used insulin needle from a friend with known hepatitis C. Anti-HCV antibodies were
positive and a viral load of 11,413 (4.1 log) copies was noted on RNA quantitative PCR testing. HCV genotyping
showed genotype 3 disease. Additional workup for etiologies of chronic liver disease included testing for autoimmune
hepatitis, Wilson’s Disease, hemochromatosis, and alpha-1-antitrypsin deficiency, all of which were negative. The
patient’s hospital course was otherwise unremarkable and his symptoms and labs improved with symptomatic cares
only. The patient’s symptoms and pattern of LFT abnormality was most likely due to acute hepatitis C infection rather
than chronic disease given the patient’s prior history and identifiable, though unique exposure prior to onset of
symptoms. The patient had spontaneous lab confirmed clearance of the virus, normalization of his LFTs and no
further symptoms.
Discussion:
Our patient is unique for several reasons. His postulated mode of transmission was highly unusual given the type of
needle and how it was used. The patient did require surgical debridement of his hand for wound management after
using his friend’s needle and thus appears to have used what is ordinarily a subcutaneous needle for deeper
penetration. The patient’s male sex and genotype-3 disease put him at higher risk of progression from his HCV
disease but the patient was able to spontaneously clear the disease without treatment.
Methods: n/a
Results: n/a
Conclusion: n/a
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Adeeti Chiplunker : ACG Member
Tarun Sharma : ACG Member
Syed Rizvi : ACG Member
Daniel Stein : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1744231
TITLE: Metabolic encephalopathy caused by combination therapy of Hepatitis C
PRESENTER: Min Win
PRESENTER (INSTITUTION ONLY): Digestive and Liver Disease Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: We present a rare case of a female patient who developed metabolic encephalopathy due to electrolyte
imbalance resulted from combination therapy of Hepatitis C.
Methods: 74 year old female presented with excessive fatigue, insomnia, headache and altered mental status. Six
weeks prior to admission, patient was started with Pegasys 180 micrograms subcutaneous weekly and Ribavirin 800
mg per oral daily for chronic hepatitis C (treatment naïve, HCV RNA 8450759 IU/ml, genotype 1a, Fibrosure test F3,
elevated ALT/AST 73/86 and normal total bilirubin, MELD score 8). 4 weeks after initial treatment, Boceprevir 800 mg
PO TID was added to combination therapy. Past medical history was significant for hypertension for which she was on
Lisinopril. No Known drug allergy. On arrival, physical examination revealed patient was hypotensive and disoriented.
Hypotension was resolved with one liter of IV fluid. Initial labs showed Hemoglobin/Hematocrit 14/41, Na 126, Cl 93,
BUN 20, Cr 0.7, Glucose 121, INR 1.2, ALT/AST/ T bil 75/82/0.9, NH3 20, lactic acid 2.0. TSH, Free T4, serum
calcium & magnesium were normal. Urine toxicology was negative. CT of head and Ultrasound of RUQ with Doppler
showed no acute changes.
Results: Hepatitis C treatment was stopped and patient was treated for metabolic encephalopathy due to electrolytes
imbalance. Her symptoms resolved completely after four days of treatment with normal saline IV infusion and
supportive care.
Conclusion: Approximately 50% of patients receiving Peginterferon and ribavirin may get flu like symptoms and one
third may experience emotional problems. Patients receiving telaprevir or boceprevir are at increased risk for
developing anemia. In addition, telaprevir is frequently associated with rashes. Metabolic encephalopathy due to
electrolyte imbalance resulted from combination therapy of Hepatitis C is very rare. 15 cases were reported that
metabolic encephalopathy occurred in chronic Hepatitis C patients up to 2013. Our case was a first one presented
with metabolic encephalopathy due to electrolyte imbalance resulted from combination therapy of Hepatitis C. Care of
patients depends upon recognition of those at increased risk for side effects, anticipation & prevention of side effects,
and appropriate response when they occur. Reduction of the dose of antiviral medications or their discontinuation may
require.
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Min Win : ACG Member
Thin Myat : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1744243
TITLE: Hemobilia due to hepatic artery pseudoaneurysm- A rare cause of Gastrointestinal bleeding in a post liver
transplant patient
PRESENTER: Sweta Kochhar
PRESENTER (INSTITUTION ONLY): Department of Gastroenterology and Hepatology, University of Arkansas for
Medical Sciences
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction:
Hemobilia is defined as hemorrhage into the biliary tract. Rupture of a hepatic artery pseudoaneurysm (HAPA) into the
hepatobiliary tract is a rare cause of hemobilia. We present a case of hemobilia due Hepatic artery pseudoaneurysm
in a post liver transplant patient.
Case presentation:A 42 year old gentleman with alpha 1 anti-trypsin deficiency underwent Orthotopic liver transplant (OLT) complicated
by anastomotic stricture requiring biliary stent placement. Three months after OLT, he presented with hematemesis
and melena. His labs showed a drop in hemoglobin from baseline of 9.5g/dL to 6.3g/dL. Liver function tests showed
cholestatic obstructive elevation.
Endoscopy with forward and side viewing endoscopes showed large clots in the duodenum. After clearing of the clots,
intermittent pulsatile bleed through the ampulla was noted, suggesting hemobilia. Previously placed biliary stent had
migrated and was visible in the distal small bowel on abdominal X-ray. Hepatic angiography was performed that
showed Right hepatic artery pseudoaneurysm. A endo vascular covered stent was placed by interventional radiology
which coveted the aneurysm and stopped the bleeding. Patient had resolution of melena with complete normalization
of Liver function tests. He was discharged home on Aspirin and Clopidogrel.
Discussion:Hepatic artery pseudoaneurysm (HAPA) is a rare vascular complication after OLT with incidence of 1%–2% and
presents with bleeding within 2 months after OLT. Luminal bleeding occurs through a fistulous tract between
aneurysm and either directly with the duodenum or indirectly via the biliary tree. Surgical, endovascular or
percutaneous approaches can be used to prevent life-threatening hemorrhage and for graft salvage. HAPA often
occurs due to anastomotic breakdown of infectious origin related to bile leak, small bowel perforation, or intraabdominal sepsis. The inflammatory milieu limits the resilience of vascular tissue resulting in mycotic
pseudoaneurysm. Other risk factors for HAPA are technical difficulty in creation of the arterial anastomosis, reexploration or repeat OLT.
Early detection with angiogram or computed tomography is crucial to avoid high mortality. Treatment options for HAPA
are through interventional radiology or surgery. Endovascular covered stenting can exclude the aneurysmal portion of
the hepatic artery while maintaining perfusion to the liver. Coil embolization can be used emergently to achieve
hemostasis but can cause ischemia to the allograft. Surgical ligation can cause ischemic injury, although resection of
the affected segment with saphenous bypass graft interposition has been described.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Sweta Kochhar : ACG Non-Member
Neelima Velchala : ACG Member
Mohit Girotra : ACG Member
Daniel Borja-Cacho : ACG Non-Member
Farshad Aduli : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1744253
TITLE: A case of Sarcoidosis presented initially with abnormal liver chemistry and subsequently developed pulmonary
symptoms
PRESENTER: Vivek Reddy Garlapati
PRESENTER (INSTITUTION ONLY): Montefiore Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: INTRODUCTION
Sarcoidosis is a multisystem disease characterized by the presence of non-caseating granulomas in affected tissue.
The common age of presentation is between 20 to 40 years. Black people are three to four times more likely to have
sarcoidosis, and may have more severe disease than Caucasians. Gastrointestinal tract involvement in Sarcoidosis is
rare, while liver involvement is common following lung and lymph nodes. Up to 35% of patients with Sarcoidosis have
abnormal liver tests and about 60 % of patients with hepatic involvement have symptoms of fever, night sweats,
anorexia and weight loss.
CASE
We present a case of a 53 year old male with comorbidities of Hypertension, Diabetes mellitus and dyslipidemia,
initially presented with elevated blood glucose level. Liver tests were noted to be abnormal (elevated alkaline
phosphatase (1021 U/L) and transaminases (AST 71 U/L and ALT 131 U/L ). Further work up including Hepatitis
panel, ANA, ASMA and AMA were negative. Chest X-ray, echocardiogram, abdominal ultrasound and MRCP were
negative for any acute pathology. Needle biopsy of liver revealed liver parenchyma with rare aggregates of histiocytic
cells consistent with non-nectrotizing granuloma.
He presented six months later with persistent cough for more than a month. In view of recent abnormal liver biopsy,
CT scan of chest was done, which revealed multiple parenchymal and subpleural nodules in a perilymphatic
distribution consistent with sarcoidosis. Whole body Gallium scan showed abnormal uptake visualized in both hila and
lungs consistent with active sarcoidosis. Angiotensin converting enzyme (ACE) level, which was initially normal (39
U/L), was found to be elevated (117 U/L) when patient presented with pulmonary symptoms. He was started on
Prednisone, and the pulmonary symptoms as well as liver enzymes improved significantly (alkaline phosphatase 170
U/L, AST 16 U/L and ALT 29 U/L) on follow up visits.
CONCLUSION
This is an interesting case of an adult male who initially was diagnosed to have hepatic Sarcoidosis without symptoms
and signs of portal hypertension. He eventually had pulmonary involvement with symptoms.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Vivek Reddy Garlapati : ACG Member
Damodar Pandey : ACG Non-Member
Hilary Hertan : ACG Member
Liver biopsy showing hepatic parenchyma with non-necrotizing epithelioid cell granuloma
IMAGE CAPTION: Liver biopsy showing hepatic parenchyma with non-necrotizing epithelioid cell granuloma
(no table selected)
AVERAGE SCORE: 4
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1744257
TITLE: Hepatotoxicity with glatiramer acetate
PRESENTER: Sharad Nangia
PRESENTER (INSTITUTION ONLY): Detroit Medical Center/Wyne State University
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Glatiramer acetate (copolymer 1) is an immunomodulator approved for treatment of Relapsing-remitting MS
(RRMS) with no known hepatotoxic effects unlike the interferon beta preparations.
We report a case of severe acute hepatitis after commencing treatment for multiple sclerosis with glatiramer acetate.
A 31-year-old female with multiple sclerosis presented with anorexia, lethargy and jaundice five weeks after
commencing glatiramer acetate. She had never received beta-interferon treatment. Investigations revealed a bilirubin
of 1.2 mg/dl AST of 879 u/L, ALT of 1215 u/L. Her liver function tests were normal before commencing glatiramer
acetate. A liver biopsy performed approximately 6 weeks after commencement of glatiramer acetate showed marked
centrilobular congestion and hemorrhage with hemosiderin laden macrophages. Mild periportal chronic inflammatory
infiltrate with scattered eosinophils. The features were not suggestive of autoimmune hepatitis but consistent with drug
toxicity. The liver tests returned to normal within a month of cessation of glatiramer acetate.
Adverse reactions should be considered in patients with liver injury and on Glatiramer therapy. Mainstay therapy
would be stopping the medication. Consideration should be given to monitoring liver function tests during long term
Glatiramer therapy. Diagnosis rests on the identification of temporal association between drug and liver injury and
exclusion of other conditions.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Sharad Nangia : ACG Non-Member
Raghu Vanama : ACG Non-Member
Pardha Devaki : ACG Member
Stephanie Judd : ACG Non-Member
Mohammad Anees : ACG Non-Member
IMAGE CAPTION:
(no table selected)
AVERAGE SCORE: 3.67
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1744301
TITLE: Hyperammonemic Encephalopathy in the Setting of Metastatic Neuroendocrine Tumor to the Liver
PRESENTER: Badr Al-Bawardy
PRESENTER (INSTITUTION ONLY): Mayo Clinic
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Hepatic encephalopathy is rare in the absence of acute liver failure, cirrhosis or collateral portosystemic
shunting. We present a case of hyperammonemic encephalopathy in the setting of diffuse liver metastasis.
Our case involves a 56 yo man with metastatic islet cell pancreatic carcinoma. He was admitted for acute confusion
and altered sleep pattern. He had no exposures to benzodiazepines, narcotics or recent gastrointestinal bleeding.
Physical examination did not reveal any signs of cirrhosis, infectious processes or neurologic deficits. Laboratory work
up was negative for both infectious and metabolic causes. Ammonia level was elevated at 174 umol/L. The rest of the
liver panel shows aspartate transaminase of 51 U/L, alanine transaminase of 32 U/L. The alkaline phosphatase was
elevated at 362 U/L with a normal bilirubin of 0.9 mg/dL. The INR and albumin were also within normal range. CT scan
of the head showed no acute intracranial pathology. Multiple liver metastases were noted on CT scan (Figure 1) and
confirmed by biopsy and octreotide scan. He was started on lactulose but continues to have intermittent hepatic
encephalopathy. He is currently being evaluated for hepatic artery embolization to reduce the tumor burden in the
liver.
In our literature search using PubMed, Web of Science and Scopus, there are only 7 reported cases of
hyperammonemic encephalopathy in the setting of metastatic neuroendocrine. Microvascular portosystemic shunting
has been proposed as the underlying mechanism that contributes to hyperammonemic encephalopathy. Hepatic
artery embolization has been shown to be an effective treatment for the encephalopathy. Our case highlights the
importance of recognizing hyperammonemia due to microvascular portosystemic shunting in the setting of metastatic
liver disease even in the absence of cirrhosis, acute liver failure, or large vessel portosystemic shunting.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Badr Al-Bawardy : ACG Non-Member
Emmanuel Gorospe : ACG Member
Shiv Desai : ACG Non-Member
Cadman Leggett : ACG Member
IMAGE CAPTION:
(no table selected)
AVERAGE SCORE: 4
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1744307
TITLE: The PATHology Less Traveled – Streptococcus Viridans Induced Liver Abscess
PRESENTER: Harneet Gahley
PRESENTER (INSTITUTION ONLY): Kingsbrook Jewish Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Streptococcus Viridans is normal flora in 90% of patients and the leading cause of dental caries. It is usually
a nonpathogenic bacterium but when it invades the bloodstream, can cause endocarditis in patients with damaged
heart valves. We present an immunocompetent patient with a hepatic abscess caused by Streptococcus Viridans
A 41-year-old male was admitted for worsening cough for one week duration. The cough was associated with a lowgrade fever and dyspnea on exertion. He also complained of headache, nausea, and generalized weakness. His
past medical history was significant for hypertension and morbid obesity. On admission, his temp was 100.6°F, BP
167/97, PR of 110, and RR of 24. On exam, crepitations were heard of the right middle to lower lung fields and his
abdomen was benign. Labs were significant for the following: Albumin 2.7g/dl, total bilirubin 2.4mg/dl, peaked levels
of alkaline phosphatase 165 U/L, alanine transferase 85 U/L, and AST 91 U/L. His WBC count was 12.6 (peaking at
16.4), and his toxicology drug screen was negative. He tested nonreactive to all hepatitis markers. A chest x-ray
delineated right basilar atelactasis while a head CT was unremarkable. An echocardiogram showed a normal EF and
no valvular lesions. Given his clinical presentation, a CT angiography was performed which was negative for
pulmonary emboli or DVT but did show 5.5cm heterogenous low-density mass in the right lobe of the liver. The
lesions measured 3.5x4.5 cm and 5.6x6.0 cm within the dome and right love of the liver, demonstrating thick irregular
enhancing capsules and central fluid intensity. It was concluded that these were probable abscess collections. The
patient underwent CT guided drainage and liver abscess aspiration. 7 ml of pus was drained from the first abscess
but the second was not anatomically amenable for drainage. The fluid drained was sent in for culture and was
determined to be Streptococcus Viridans and was started on Flagyl and Rocephin. The patient was discharged on oral
Levaquin and Flagyl for ten days and is currently doing well.
Pyogenic abscesses account for nearly 2/3 of all liver lesions. The most common overall cause is through biliary
disease such as cholangitis, followed by endocarditis; both of which were ruled out by diagnostic testing. Given the
propensity for strep viridians to cause dental caries and gingival infections we recommend a thorough oral
examination as this may be an underlying cause for pyogenic liver abscesses in patients without other etiologies. We
plan to conduct a retrospective analysis of our microbiology database to query the incidence of oral flora in the
pathogenesis of pyogenic liver abscesses.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Harneet Gahley : ACG Non-Member
Arjun Bhansali : ACG Non-Member
Niket Sonpal : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.67
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1744310
TITLE: A Rare Case of Hepatocellular Carcinoma After Liver Transplantation in Primary Sclerosing Cholangitis
PRESENTER: Bonnie Ewald
PRESENTER (INSTITUTION ONLY): Tufts Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Primary sclerosing cholangitis (PSC) is associated with increased risk of cholangiocarcinoma (CCA) and, to
a lesser extent, hepatocellular carcinoma (HCC). Liver transplantation is the only potentially curative treatment in
patients with end stage liver disease resulting from PSC. Recurrence of the disease has been reported in 20-25% of
patients within 5-10 years of transplantation. Incidence of hepatobiliary malignancy in patients who have undergone
transplantation for PSC is not widely reported in the literature. We report a case of a 50 year old male, previously
diagnosed with PSC at age 20, who underwent orthotopic liver transplantation due to progressive liver failure and was
found to have HCC 24 years post transplant. After transplantation, he was treated with prednisone, methotrexate, and
cyclosporine, which were discontinued due to recurrent squamous cell carcinoma of the skin and he was subsequently
maintained on mycophenolate mofetil. He developed recurrent PSC 8 years post transplant as well as episodic
bacterial cholangitis which was treated with chronic rotating antibiotics and ursodiol. Liver enzymes prior to his
presentation were stable and imaging from 4 years prior to his diagnosis of HCC showed no notable lesions. This
patient was admitted to the hospital after a mechanical fall resulted in a femoral fracture. He developed a fever to
38.7°C and leukocytosis. On presentation, he denied history of abdominal pain, jaundice, and weight loss. Physical
exam was significant for liver edge palpated 3 cm below the costal margin without jaundice, abdominal pain, or
distention. His LFTs were elevated (AST 43 IU/L, ALT 55 IU/L, Alk Phos 445 IU/L, total bilirubin 1.8 mg/dL, direct
bilirubin 1.3 mg/dL) and due to concern for recurrent bacterial cholangitis, the patient underwent magnetic resonance
cholangiopancreatography which showed a 6.1 cm by 5.3 cm heterogeneous mass containing hemorrhage and
necrosis in the medial segment of the left hepatic lobe. A biopsy demonstrated poorly differentiated HCC. Further
laboratory testing revealed a normal AFP (<2.0), elevated CEA, Ca 19-9, and Ca 125 at 4.1 ng/mL, 262 U/mL, and
143 U/mL, respectively. Published reports of screening for malignancy in PSC are limited by a relatively low incidence
of this disease. Literature regarding the utility of CCA surveillance provides conflicting clinical recommendations and
furthermore, HCC surveillance is currently not recommended due to the low incidence. We present a rare case of
HCC in PSC after liver transplantation. Further investigation is needed to determine the incidence of heptobiliary
malignancy and thus the benefit of cancer surveillance in patients with PSC after transplantation.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Bonnie Ewald : ACG Non-Member
Kathleen Viveiros : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3.67
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1744396
TITLE: Rescue therapy with hypernatremia/hypothermia protocol in transplant-ineligible patients with advanced
cerebral edema from acetaminophen toxicity: case series from tertiary care center
PRESENTER: Tossapol Kerdsirichairat
PRESENTER (INSTITUTION ONLY): University of Minnesota
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: The prevalence of acute liver failure is increasing and acetaminophen is still the leading cause in the West
and generates the highest risk of developing cerebral edema. Only around 53% of patients with acute liver failure are
ever listed for transplant and as many as 25% of listed patients die awaiting transplantation. There is only one case
report using combined hypernatremia and hypothermia therapy in a patient not eligible for liver transplantation. We
report our 5-year experience on advanced cerebral edema and impending cerebral herniation in transplant-ineligible
patients with fulminant liver failure secondary to acetaminophen toxicity.
Case 1: A 29-year-old female with a past medical history of depression presented with encephalopathy, and severe
coagulopathy, and reported acetaminophen overdoing 24 hours. She was a Jehovah’s Witness and her family refused
to consent to liver transplantation.
Case 2: A 37-year-old female with a past medical history of ongoing alcohol dependence, with a similar presentation.
Given refractory alcoholism, she was considered not a candidate for liver transplantation.
Both patients were at highest risk for brain edema as they developed coma, serum ammonia greater than 100
micromol/L, hyperacute progression of liver failure, the need for vasopressors, and renal replacement therapy. Their
neurological status deteriorated with signs of impending central herniation including extensor posturing, sustained
clonus, and bilateral Babinskis. Brain CT confirmed brain edema in both cases. Both patients could not receive
intracranial pressure monitoring (blood transfusion was refused in Case 1 and severe intractable coagulopathy in
Case 2). In an effort to avoid catastrophic neurologic sequelae, hypernatremia (sodium 145-150 mmol/L) and
hypothermia (32 °C) were urgently initiated. Timing of rewarming was based on neurologic findings, liver function, and
findings on serial CT brain. Case 1 received the protocol for 1 day while this was prolonged to 6 days in Case 2. Both
patients were safely discharged home with complete neurologic recovery on hospital day 20 and 32, respectively.
While liver transplantation is the treatment of choice for fulminant liver failure secondary to acetaminophen toxicity, a
hypernatremia/hypothermia protocol can be successfully used as a rescue therapy in addition to standard of treatment
(hyperventilation, N-acetylcysteine, and ICU status) in selected patients with severe brain edema from acute liver
failure who are transplant-ineligible, but have good potential for liver recovery.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Tossapol Kerdsirichairat : ACG Member
John Lake : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1744422
TITLE: Telaprevir Induced Drug Rash with Eosinophilia and Systemic Symptoms (DRESS) Syndrome
PRESENTER: Rabab Hajar
PRESENTER (INSTITUTION ONLY): Nassau University Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Telaprevir has been increasingly used in combination with pegylated interferon and ribavarin for the
treatment of chronic hepatitis C, genotype 1. Skin rash is the most common side effect of telaprevir, as it can occur in
56% of patients compared to 34 % taking ribavarin or interferon alone. It is usually mild in nature and rarely a cause of
treatment cessation. However about 3.7 % of patient have reported severe rashes sometimes requiring
discontinuation of the medication. We present a case of drug-induced rash with systemic eosinophilia (DRESS)
syndrome secondary to telaprevir use.
A 56 year-old Caucasian male with history of chronic HCV, genotype 1a, presented to the medical emergency room
with complaints of fatigue and the presence of a generalized rash. He had been started on treatment with pegylated
interferon, telaprevir, and ribavarin 10 weeks prior. On initial triage, the patient’s blood pressure was 113/60 mm Hg,
and body temperature was 100.3 degrees Fahrenheit. Physical examination was remarkable for an exanthematous
rash on his trunk and limbs with some few dispersed pustules on his neck and chest. There was significant cervical
lymphadenopathy, along with trace pedal edema bilaterally. Laboratory results revealed leukocytosis, with a white
blood cell count of 13.8 with 30% eosinophils, and a serum creatinine of 1.6 mg/dL. Given the history of telaprevir use
and the new onset of a rash with a profound eosinophilia, along with what appeared to be systemic involvement, the
diagnosis of DRESS syndrome was made. The patient was started on systemic steroids, and telaprevir was
immediately discontinued. Over the next few days, the patient noted a marked improvement in his skin rash, and
laboratory parameters including eosinophilia, and creatinine returned to baseline.
In rare instances, telaprevir use can lead to the progression of DRESS syndrome; a serious and potentially fatal drug
reaction. DRESS syndrome can manifest as general exanthema, fever, generalized lymphadenopathies, eosinophilia
or atypical lymphocytosis and end organ damage. Mortality rates from DRESS syndrome can be as high as 10 %.
DRESS syndrome may often pose a diagnostic challenge, as skin eruptions and varied organ involvement may differ
in patients. Clinicians should maintain a high index of suspicion for DRESS syndrome in patients treated with
telaprevir that present with new skin lesions, fever, and the development of systemic symptoms or evidence of endorgan damage. Treatment includes prompt withdrawal of the drug and initiation of corticosteroids. In severe cases, the
initiation of intravenous immune globulins may be the treatment of choice.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Dhyan Rajan : ACG Non-Member
Rabab Hajar : ACG Non-Member
Jaspreet Singh : ACG Non-Member
Prakash Viswanathan : ACG Non-Member
Krishnaiyer Subramani : ACG Non-Member
Kaleem Rizvon : ACG Non-Member
Paul Mustacchia : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1744456
TITLE: " Cryptococcal Meningitis Presenting with Alerted Mental Status in a Patient with Cirrhosis: Diagnostic
Dilemmas "
PRESENTER: Saba Farooq
PRESENTER (INSTITUTION ONLY): UTHSC
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Abstract: Altered mental status is a frequent reason for admission for patients with cirrhosis and is usually
caused by hepatic encephalopathy. In this abstract we report a patient with cirrhosis, who was admitted with altered
mental status and eventually found to have cryptococcal meningitis.
Case Report: 48 year old AA female, with cirrhosis caused by NASH, was admitted with suspected hepatic
encephalopathy. Vital signs showed a temperature of 38.4°C, heart rate of 82 /min, blood pressure of 110/70 mmHg,
and respiratory rate of 19 /min. On neurological exam she was not oriented to time, place and person and had no
signs of meningism. She did not have any focal neurological signs. Labs: AST/ALT: 46/118, Alk Phos: 251, INR: 1.5,
ammonia level was elevated at 52 umol/L. Her electrolytes and renal functions were within normal range. Her MELD
was 13 and she had Child Pugh class B. Blood cultures remained negative for any microbial growth. Her HIV test was
negative.She was promptly started on lactulose and started having adequate bowel movements. However, her mental
status deteriorated over the next 72 hours and a lumbar puncture (LP) was performed. CSF studies showed a WBC
count of 1875 cells/mm3( 69 % neutrophils, 30% lymphocytes) , glucose of 30mg/dl, protein 50mg/dl and cryptococcal
antigen titer of 1:8. CSF cultures grew Cryptococcus neoformans and she was started on liposomal amphoterecin B.
She responded well to treatment with remarkable improvement in mental status.
Discussion: Cryptococcus neoformans meningitis is very uncommon in patients with cirrhosis. Unless the clinician
keeps a high index of suspicion it can be easily missed; especially since every patient with altered mental status is
labeled as hepatic encephalopathy. Moreover, LP is difficult in cirrhotic patients due to coagulopathy and
thrombocytopenia, potentially delaying or preventing the diagnostic studies such as CSF culture or crytococcal
antigen. While serum crytococcal antigen test is not very sensitive and false positive tests can occur (in infections with
Trichosporon asahii fungus or Stomatococcus and Capnocytophaga bacteriae), one might have to rely solely on
serum antigen for a diagnosis in many patients with severe coagulopathy. This diagnostic dilemma is further
accentuated by potential toxicities of fungicidal drugs, (Amphotericin B and/or Flucytosine) in patients with
compromised hepatic function and reduced renal function secondary to hepatorenal syndrome.
Conclusion: Cryptococcal meningitis can masquerade as hepatic encephalopathy in patients with cirrhosis. A high
clinical suspicion along with early initiation of diagnostic studies and therapies are needed for effective treatment.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Saba Farooq : ACG Non-Member
Fazal Yahya : ACG Non-Member
Umair Sohail : ACG Member
Mohsin Haseeb : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.33
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
David Hass: [No Comments]|Charlene Le Pane: [No Comments]|Renee Young: [No Comments]|Rowen Zetterman:
[No Comments]
CONTROL ID: 1744492
TITLE: A unique case of Primary Hepatic Neuroendocrine Carcinoma causing Fulminant liver failure.
PRESENTER: Mandeep Singh
PRESENTER (INSTITUTION ONLY): Albany Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: We report a rare case of primary hepatic neuroendocrine carcinoma (PHNEC) causing fulminant liver failure
in a young male.
34 y/o healthy AA male presents with one week of severe RUQ abdominal pain, jaundice and non-bloody diarrhea.
Vitals noted a temp- 98 F, BP 100/60, HR- 108, RR 24 and pulse ox 98 % on 2L oxygen. Physical exam revealed
yellowing of the skin, scleral icterus, RUQ tenderness, and hepatomegaly. Labs revealed significant leukocytosis with
neutrophilia, mild microcytic anemia, sodium 121, chloride 82, bicarbonate 20, total bilirubin (Tb) 11.6, direct bilirubin
7.2, ALP 416, AST 546, ALT 318, albumin 3.1, INR 1.3, LDH 1858, lactic acid 9.8. An abdominal US revealed
hepatomegaly with heterogeneous echo pattern, gallbladder wall thickening, CBD dilation at 0.8cm, ascites, and
findings concerning for hepatic vein thrombosis. CT-abdomen with liver mass protocol confirmed above findings.
Patient was then transferred to ICU and started on IV heparin, broad spectrum antibiotics and vasopressors for
hypotension. He had progressive worsening of LFT’s with AST/ALT 4132/1273, Tb 15.5.and INR 1.9. Hepatitis A, B,
and C serology were negative and serum acetaminophen and salicylate levels were normal. N-acetylcystine started
for worsening liver failure. Later, he developed AKI with severe metabolic acidosis and was started on CRRT.
Transjugular hepatic venogram and liver biopsy were performed. Venogram demonstrated no filling defects to
suggest thrombus. Patient was then transferred to a transplant center for a potential liver transplant. He suffered a
fatal cardiopulmonary arrest on the following day. Liver biopsy revealed tumor, immunoreactive with vimentin and
focally with synaptophysin consistent with poorly differentiated non-small cell carcinoma with neuroendocrine
differentiation.
Despite an increase in the incidence of neuroendocrine tumors, PHNEC remains a rarity. Among the reported cases,
the highest incidence was in the fifth decade. Diagnosis is an evolution, and requires a systematic clinical exclusion
with histological confirmation. Surgical resection is effective, safe and prognosis is excellent despite a high recurrence
rate. No clear indication for liver transplantation exists, but can be considered in patients with unresectable lesions.
Disease progression is usually slow, but our patient deteriorated rapidly with multi-organ failure that was fatal.
Methods: n/a
Results: n/a
Conclusion: n/a
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Mandeep Singh : ACG Member
Pratyusha Parava : ACG Non-Member
Jesse Green : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 5.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: [No
Comments]
CONTROL ID: 1744493
TITLE: Sick Patients with an Unclear Etiology of Hepatic Dysfunction: Think Hemophagocytic Lymphohistiocytosis
(HLH)
PRESENTER: Kara De Felice
PRESENTER (INSTITUTION ONLY): Mayo Clinic
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Hemophagocytic lymphohistiocytosis (HLH) mimics infections, hepatitis, and systemic illnesses. Diagnostic
criteria requires five of the following: fever, hepatitis, splenomegaly, cytopenia (≥ two cell lines), hypertriglyceridemia
and/or hypofibrinogenemia, hemophagocytosis (bone marrow ,spleen, or lymph node), low or absent natural killer
(NK) cell activity, serum ferritin >500 µg/L, and sIL-2 receptor >2400 U/mL. In the absence of chemotherapy with
dexamethasone, etoposide, and cyclosporine (HLH-94 protocol) outcome is fatal. Case 1: 57-year-old woman
presented with fevers, night sweats, weight loss, and abdominal pain. Labs revealed pancytopenia, alkaline
phosphatase 564 U/L, AST 108 U/L, ALT 24 U/L, and total bilirubin 0.7 mg/dL. Imaging showed hepatosplenomegaly.
A liver biopsy showed periportal hepatitis with hemophagocytosis. NK cell activity was low, ferritin 3972 mcg/L, sIL-2
receptor 20820 U/ml, and bone marrow hypercellular with erythrophagocytosis. She responded well to the HLH-94
protocol. Case 2: 60-year-old woman with pure red cell aplasia secondary to parvovirus presented with night sweats,
fevers, weight loss, arthralgias, salmon-colored rash, and jaundice. Labs revealed normocytic anemia, ferritin 58300
mcg/L, AST 1205 U/L, ALT 1056 U/L, alkaline phosphatase 355 U/L, total bilirubin 9.0 mg/dL, and negative ANA and
RF. Imaging revealed hepatosplenomegaly. Liver biopsy showed panacinar hepatitis, cholestasis, and rare
erythrophagocytosis. She fulfilled the Yamaguchi criteria for Still's disease and was treated with IVIG and steroids with
no improvement. Therefore, a repeat bone marrow biopsy was performed which showed red cell aplasia and
erythrophagocytosis. NK cell activity was absent and the patient was diagnosed with HLH. She was treated with the
HLH-94 protocol with significant improvement. Case 3: 28-year-old man presented with fevers, sore throat, fatigue,
and cervical lymphadenopathy. Imaging revealed diffuse lymphadenopathy. Labs showed pancytopenia, alkaline
phosphatase 319 U/L, AST 357 U/L, ALT 410 U/L, total bilirubin 5.9 mg/dL, and ferritin 5476 mcg/L. An infectious
workup revealed EBV viremia. A liver biopsy showed panacinar hepatitis with histiocytes. Lymph node FNA revealed a
T-cell lymphoproliferative disorder with EBV positivity. A bone marrow biopsy was hypocellular with hemophagocytic
cells. NK cell activity was low and sIL-2 receptor elevated at 20900 U/ml. The patient was diagnosed with HLH and is
currently undergoing treatment with the HLH-94 protocol.
Methods: N/A
Results: N/A
Conclusion: HLH should be suspected in rapidly deteriorating patients with hepatic dysfunction and multi-system
disease. Early diagnosis and treatment with the HLH-94 protocol has favorable outcomes.
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Kara De Felice : ACG Member
Patrick Kamath : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: [No
Comments]
CONTROL ID: 1744575
TITLE: A Rare Case of Macro-AST
PRESENTER: Shivali Berera
PRESENTER (INSTITUTION ONLY): University of Miami Miller School of Medicine
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Isolated chronic elevation of serum aspartate aminotransferase (AST) activity in the absence of organspecific disease may be due to the presence of a macro-enzyme form of AST complexed with immunoglobulin
(macro-AST). We describe a case of a young woman referred to our clinic for isolated AST elevation and chronic
fatigue.
A 29-year-old Colombian woman with no significant medical history initially presented to an outside facility with
abdominal pain and was noted to have an isolated AST elevation of 605 IU/L in August of 2011. The patient did not
endorse history of fever, jaundice, weight loss, strenuous exercise, heavy alcohol use, or pesticide exposure but had
taken Chinese herbal supplements two years prior. Physical examination did not reveal any obvious abnormalities
with anicteric sclera, benign abdominal exam without hepatosplenomegaly, and no edema. The patient's symptoms
resolved, but AST levels fluctuated between 88 IU/L and 725 IU/L with ALT levels remaining between 6 and 21 IU/L.
Lipid panel, creatinine kinase, TSH, CRP, and iron studies were normal. Additional laboratory tests were normal or
negative including ceruloplasmin, alpha-1 antitrypsin, autoimmune markers- anti-nuclear, anti-mitochondrial, antismooth muscle, anti-transglutaminase, and anti-gliadin antibodies, immunoglobulins, aldolase, creatinine kinase,
celiac panel, Lyme disease, selenium, and hepatitis A, hepatitis B, and hepatitis C antibodies. Studies identified IgG
antibodies to Epstein-Barr virus and cytomegalovirus, without detectable IgM. Abdominal ultrasound and MRCP were
negative, and liver biopsy showed inflammation with two readings of grade 1 disease.
After exclusion of other processes, polyethylene glycol (PEG) precipitation study was performed, consistent with the
presence of macro-AST with 99% of activity precipitated with PEG.
This is a rare entity with more than 60 cases reported in literature. The role of resolved EBV infection as a potential
cause of macro-AST development is questioned in similar case reports of isolated AST elevation. Compared to gel
filtration chromatography, identification with PEG precipitation is inexpensive, less labor-intensive, and performable in
most laboratories. PEG causes increased protein concentration and precipitation by withdrawing solvent molecules
from immunoglobulins, proteins and lipids. While the pathogenesis of this immune-complex development is unknown,
the disease appears to be benign with minimal or no progression to advanced liver disease. Awareness and early
recognition of macro-AST will avoid invasive or costly investigations, encourage availability of laboratory testing, and
allow for further study of the natural history of this disease process.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Shivali Berera : ACG Non-Member
Jahnavi Naik : ACG Member
Adam Peyton : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.67
REVIEWER FLAGS: Haritha Avula - Conflict of Interest: 1
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: [No
Comments]
CONTROL ID: 1744945
TITLE: Severe Hepatitis leads to the diagnosis of DRESS Syndrome.
PRESENTER: Trinadha Pilla
PRESENTER (INSTITUTION ONLY): Southern Illinois University School of Medicine
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Intoduction: Drug reaction with eosinophilia and systemic symptoms (DRESS) is a rare and severe
idiosyncratic reaction to a drug that is characterized by a long latency of onset after exposure to the offending
medication. It was first recognized as early as 1959 however the term was coined in a 1996. Apart from the skin and
hematologic manifestations liver is the main organ involved with features of severe hepatitis.
Case Report: A 38-year old man presented with a rash over his chest and abdomen that spread to his back and
extremities. He had fever, chills, right abdominal pain, nausea, vomiting, diarrhea and dark urine. The rash was
erythematous, pruritic and painful and spread to the whole body including his palms and soles. The eruption was
maculopapular at onset, which desquamated in the next 3 days and changed to exfoliative dermatitis. He finished a
course of trimethoprim/sulfamethoxazole 2 weeks back for prostatitis. He had generalised tender lymphadenopathy,
jaundice and tender hepatomegaly. A CT-scan and ERCP of the abdomen revealed features of acute cholecystitis
and mild erosive gastritis. He was noted to have eosinophilia on CBC and marked elevated liver transaminases (ALT:
1341, AST: 612, total bilirubin: 8.2 and Alkaline phosphate: 353). He underwent cholecystectomy. Hepatitis virus panel
and HIV were negative. EBV IgG was positive and IgM was negative. Additionally, ANA, Anti-mitochondrial antibodies
were negative. Anti smooth muscle antibody titer was positive at 1:40.
A liver and skin biospy was performed. Skin biospy revealed positive fibrinogen staining throughout the dermis with
negative skin immunofluorescence indicating a vasculitis. Liver biopsy revealed an eosinophilic and lymphocytic
infiltrate with granulomas on grocott's methenamine silver stain and acid fast bacilli stains were negative. Gall bladder
biopsy showed lymphoid follicles. He was finally diagnosed with DRESS syndrome due to exposure to
trimethoprim/sulfamethoxazole. He was started on topical triamcinolone and oral prednisolone at the dose of 1
mg/kg/day for 2 weeks, which was tapered over a period of next 4 weeks. The patient showed rapid resolution of
fever, eosinophilia and progressive improvement in skin rash and liver dysfunction over a period of 3 weeks.
Discussions: DRESS syndrome is a rare cause of hepatitis. DRESS syndrome usually begins several weeks after
exposure to the offending drugs such as trimethoprim/sulfamethoxazole, phenytoin, phenobarbital, carbamazepine
and lamotrigine among others. Treatment consists of stopping the offending medication and providing supportive care.
High dose steroids have also been used. Overall mortality in DRESS syndrome is about 10%.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Trinadha Pilla : ACG Non-Member
Sidharth Chandra : ACG Non-Member
Daniel Ryan : ACG Non-Member
Swapna Devanna : ACG Non-Member
Dheeraj Reddy : ACG Non-Member
Aman Ali : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: [No
Comments]
CONTROL ID: 1744953
TITLE: Acute Hepatic Failure Due to Legionnaire’s Disease
PRESENTER: Rizwan Jafri
PRESENTER (INSTITUTION ONLY): Franciscan St. James Hospital
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction:
We report a case of acute hepatic failure associated with legionnaire’s disease in a 41 y.o. male who presented with
weakness and jaundice.
Case:
A 41 year old male with no significant past medical history presented to the hospital with complaints of dizziness,
weakness, and jaundice noticed by his PCP. He had a one day history of fevers, chills, increased urinary frequency,
and decreased appetite. Initial labs revealed transaminitis, hyperbilirubinemia, and leukocytosis. He was also febrile to
103.5 F and hyperglycemic. A CT of the chest showed large volume of consolidation in the right lower lobe and a right
pleural effusion. A right upper quadrant ultrasound was negative for portal vein thrombosis. Work up for infectious
etiologies was positive for legionalla antigen. He was admitted to the intesive care unit for further management.
Discussion:
Pneumonia is the predominant clinical manifestation of Legionella infection. Extrapulmonary manifestations can exist,
most commonly gastrointestinal symtpoms such as nausea, vomiting, diarrhea, and abdominal pain. Although liver
function tests are frequently abnormal in Legionnaires' Disease, jaundice occurs rarely except as a terminal event. Our
patient presented with jaundice and weakness as his initial symptoms and eventually developed hypoxia and
respiratory failure requiring intubation. This case suggests that the clinical manifestation of Legionella can consist of
extrapulmonary manifestations, such as jaundice in our patient, as the primary presenting symptom. Mortality of
community-acquired Legionnaires' disease ranges from 16 to 30 percent if untreated or treated with inactive
antibiotics. We hope to bring this rare presentation of the disease to the attention of most clinicians so as to prevent
delay in diagnosis and treatment.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Rizwan Jafri : ACG Member
Yameen Rashid : ACG Member
Farhoud Khosravi : ACG Member
Alex Yarbrough : ACG Member
Gopichand Naguboyina : ACG Non-Member
Mustafa Nawaz : ACG Member
Fares Hamad : ACG Member
Faizan Khan : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: I
could not find much in literature on abnormal liver tests and liver failure due to Legionnaire's disease?Questionable
association?
CONTROL ID: 1744958
TITLE: Disulfiram induced fulminant hepatic failure
PRESENTER: Samyuktha Ramavaram
PRESENTER (INSTITUTION ONLY): Department of Gastroenterology and Hepatology, University of Arkansas for
Medical Sciences
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction:
Disulfiram has been used as an adjunct therapy in treatment of chronic alcoholism. Disulfiram induced liver injury can
range from asymptomatic elevations in serum aminotransferases, to symptomatic liver injury with jaundice and rarely
fulminant hepatic failure and death. We present a rare case of disulfiram induced fulminant hepatitis.
Case presentation:
A 66 year old male with history of Hypertension, Diabetes Mellitus and Atrial fibrillation on Coumadin was admitted
with acute liver failure. He had a history of heavy alcohol use and decided to quit alcohol 3 weeks prior to admission.
He was started on Disulfiram but did not tolerate the medication and stopped it 10 days prior to current admission. He
presented with hypoglycemia and was found to have elevation of liver enzymes with Total Bilirubin of 13, AST of 2749,
ALT of 3423 and Alkaline phosphatase of 293. INR was greater than10. Work up was negative for acute viral
hepatitis,tylenol and salicylate toxicity. Coagulopathy initially reversed with vitamin K and was felt to be due to
Coumadin toxicity. There was no evidence of encephalopathy on admission. However, INR continued to remain
elevated even after discontinuing Coumadin. CT did not show cirrhosis but showed evidence of portal hypertension.
He was started on N-Acetylcysteine protocol for acute liver failure. Liver function tests (LFTs) continued to increase
with bilirubin peaking at 36 mg/dl. Liver biopsy was planned but deferred as patient developed fulminant hepatitis. He
was not a liver transplant candidate due to recent alcohol use. Encephalopathy and coagulopathy continued to worsen
and family opted for Hospice.
Discussion:
Disufiram has been used in treatment of chronic alcoholism since 1948. It inhibits acetaldehyde dehydrogenase
enzyme leading to accumulation of acetaldehyde. This leads to flushing, tachycardia, nausea, vomiting and confusion.
Chronic therapy with disulfiram is associated with mild aminotransferase elevations but elevations above 3 times the
upper limit of normal (ULN) occur in upto 4% of patients. Liver injury usually occurs within 2 to 12 weeks of starting
disulfiram, but latency period tends to be shorter in cases of re-exposure. The clinical presentation of disulfiram
induced hepatotoxicity resembles acute viral hepatitis. In severe injury, the fatality rate is at least 10%. Histologically,
findings include focal hepatocellular necrosis, lobular disarray and chronic inflammatory cell infiltrates with eosinophils.
Conclusion:
Disulfiram induced hepatotoxicity is associated with high mortality and should lead to immediate discontinuation of the
drug. If stopped early, complete recovery is expected within 4 to 6 weeks.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Samyuktha Ramavaram : ACG Non-Member
Neelima Velchala : ACG Member
Mohit Girotra : ACG Member
Farshad Aduli : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: [No
Comments]
CONTROL ID: 1745025
TITLE: An Unusual Cause for Portal Hypertension
PRESENTER: Mary Anne Chacko
PRESENTER (INSTITUTION ONLY): Methodist Dallas Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: The patient was a 53 year old female with PMH of hepatitis C after orthotopic liver transplant, transjugular
intrahepatic portosystemic shunting, idiopathic thrombocytopenic purpura (ITP), and atrial fibrillation. She developed
recurrent hepatitis C after transplant that was complicated by ascites and severe thrombocytopenia, which was treated
with eltrombopag. She was admitted to an outside facility with large ascites and three episodes of hematemesis
resulting in 3L blood loss. She was transfused with 14 units of pRBCs. She underwent emergent
esophagoduodenoscopy which indicated esophageal varices and three bands were placed.
Physical exam showed large abdominal ascites.
Laboratory results included WBC 6, Hgb 9.5, Hct 27.6, Platelets 15, AST 1761, ALT 508, Alkaline phosphatase 49,
Albumin 2.2, PT 16, INR 1.3.
Imaging and Procedures:
Abdominal ultrasound indicated potential portal venous thrombosis. Subsequent abdominal CT showed arteriovenous
fistulas. The patient underwent hepatic arteriogram which showed numerous hepatic artery to portal vein fistulas
which could have caused the elevated portal pressures. The patient underwent coil embolization of the dominant
fistulas but there were too many small fistulas for complete embolization. The patient also underwent splenic
embolization for thrombocytopenia. She had another arteriogram after one week with repeat coil embolization of one
of the larger fistulas. However, the patient remained at risk for increased portal pressure and GI bleed due to the
smaller, non-embolized fistulas. Three paracenteses were performed with a total of 12.85 L of ascites drained. Initial
fluid analysis showed no peritonitis but paracentesis after arteriogram and splenic embolization showed peritonitis.
She was placed on antibiotics.
The patient’s condition stabilized and she was extubated the day after admission. She had a history of ITP and
successful treatment with eltrombopag which was subsequently discontinued due to side effects. The decision was
made not to restart eltrombopag and to transfuse platelets as required. Eventually 12 units of leukocyte reduced
pheresis platelets were transfused. The upper GI bleed was stable after banding of esophageal varices and treatment
with octreotide and esomeprazole.
Conclusion
Arterioportal fistula is an unusual contributive cause for portal hypertension and is usually associated with trauma.
Our patient presented with an unusual case of numerous such fistulas that may have eluded diagnosis had ultrasound
and CT abdomen not been followed by arteriogram. Embolization was the most effective option for addressing this
problem.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Mary Anne Chacko : ACG Non-Member
Leslie Cler : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: [No
Comments]
CONTROL ID: 1745049
TITLE: An Unusual Case of Multiple Myeloma Diagnosed Due To Clinical Manifestations Of Infiltration Of The Disease
Into The Liver
PRESENTER: Victor Velocci
PRESENTER (INSTITUTION ONLY): Providence Hospital
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Abstract
Clinical manifestations of infiltration of multiple myeloma into the liver are extremely rare. We present a case of a 73year-old African-American female presenting with complaints of persistent nausea and vomiting. Initial laboratory
findings included BUN of 23, creatinine 2.3, AST 73, ALT 59, alkaline phosphatase 335, total bilirubin 1.3 mg/dL and
direct bilirubin 0.7mg/dL. Serologic abnormalities persisted prompting CT guided biopsy of the liver. Pathology
demonstrated diffuse plasma cell infiltration and further workup confirmed the diagnosis of multiple myeloma.
Case Report
A 73-year-old female presented with complaints of nausea and vomiting of 3 weeks' duration with associated
intermittent diarrhea. Physical examination revealed a soft, nondistended abdomen, positive for periumbilical and
epigastric tenderness with no guarding or rebound. Laboratory results were significant for a BUN of 23, creatinine 2.3,
AST 73, ALT 59, alkaline phosphatase 335, total bilirubin 1.3 mg/dL, direct bilirubin 0.7mg/dL and CA 19-9 of 352.7.
Abdominal ultrasound, endoscopic ultrasound, and MRI of the abdomen with and without contrast was employed but
could not explain persistent elevation in the patient’s transaminases, alkaline phosphatase and bilirubin. CT guided
biopsy of the liver was ordered. Findings of myelomatosis, an atypical plasmacytic infiltration of the liver was
described per the pathology. Serum and urine electrophoresis showed a lambda light chain predominance, with levels
found to be 930mg/dL and 1960mg/dL. Bone marrow aspiration confirmed a 17% marrow plasmacytosis, lambda
restricted. The patient was diagnosed with multiple myeloma and started on treatment with bortezomib and
dexamethasone.
Discussion
Extraosseous involvement of multiple myeloma is a well-documented manifestation of the disease. Infiltration of the
liver has been described in the literature with Walz-Mattmüller et al. reporting liver involvement in 32% of patients with
multiple myeloma (1). Although liver infiltration and abnormalities in liver function tests are common, clinical
manifestations of these irregularities are exceedingly rare (2). These instances exist in the literature as case reports,
such as that described by Barth et al. involving a patient presenting with acute cholestatic hepatitis diagnosed with
multiple myeloma on biopsy of the liver (3). We report a similar case in which a patient with complaints of nausea and
vomiting and obstructive cholestasis on serology was subsequently diagnosed with multiple myeloma. Although rare,
manifestations of liver infiltration can occur and physicians should remain vigilant in the workup of cholestatic jaundice
not explained by other pathology.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Victor Velocci : ACG Non-Member
Mohammed Nasser : ACG Non-Member
Roberto Gamarra : ACG Non-Member
Rajendra Manam : ACG Non-Member
William Sharp : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3.5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: [No
Comments]
CONTROL ID: 1745149
TITLE: Safety of combined use of Pegylated interferon and Ribavirin along with Anti-TNF alpha in patients with
Hepatits C and Rheumatological disorders.
PRESENTER: Sohail Ashraf
PRESENTER (INSTITUTION ONLY): Manchester Royal Infirmary
PRESENTER (COUNTRY ONLY): United Kingdom
ABSTRACT BODY:
Purpose: Use of anti TNF-alpha with antiviral treatment in patients with Rheumatological disorders and concomitant
Hepatitis C infection raises concerns with regards to immunosuppression and flare of Hepatitis C virus or lack of viral
clearance. The objective of this study was to monitor the Hepatitis C viral response and any superimposed side effects
of the combined treatment in our patients.
Methods: We describe 2 patients with Ankylosing Spondylitis and concomitant Hepatitis C infection who were on Anti
TNF alpha therapy and were treated with Pegylated Interferon plus Ribavirin in a tertiary care Liver Unit.
Results: One patient was on Adalimumab for Ankylosing Spondylitis who received 6 months of Pegylated Interferon
and ribavirin for Genotype 3 Hepatitis C infection without liver fibrosis and achieved sustained virological response
without significant cytopenia or viral breakthrough. While the second patient is receiving same antiviral treatment for
Genotype 1 hepatitis C infection while being on Etanercept for Ankylosing Spondylitis. He achieved undetectable HCV
RNA at week 24 without significant side effects.
Conclusion: Treating Hepatitis C patients with Pegylated Interferon and Ribavirin while receiving Anti-TNF alpha
appears to be safe and doesn’t relate to lack of Hepatitis C clearance though careful monitoring is needed.
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: Yes
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Sohail Ashraf : ACG Non-Member
Narendra Kochar : ACG Non-Member
Martin Prince : ACG Non-Member
Shaun Greer : ACG Non-Member
Esther Pears : ACG Non-Member
Jessy Joesph : ACG Non-Member
Annita Mcnicholas : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3.5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: [No
Comments]
CONTROL ID: 1745236
TITLE: Unusual cause of GI bleed, coagulopathy and elevated liver related tests in young male
PRESENTER: Ghulamullah Shahzad
PRESENTER (INSTITUTION ONLY): Nassau University Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: 21 year-old male presented with intermittent fevers and 10 pound weight loss for two months and black tarry
stools for two days. He denied any abdominal pain, recent travel or sick contacts. His vitals were significant for
tachycardia and fever of 102F. His rectal examination showed no masses, normal sphincter tone, hem-negative stools
and external hemorrhoids. His wbc count was 0.91, hemoglobin was 9.8, platelets of 92. His ALT 198, AST 265, AP
238, TB 1.1, TP 7.1, albumin 3.6, and INR 1.4. Further work up included ferritin 17636, LDH 1324, triglycerides 237
and elevated CRP/ESR with low fibrinogen. His HIV, hepatitis panel, EBV, CMV, HSV, RPR, PPD, influenza A/B, viral
respiratory culture, brucella, bartonella, his abdominal US and CT abdomen/pelvis showed only splenomegaly. Bone
marrow biopsy showed pancytopenia, megakaryocytes, no fibrosis, cellular infiltrates or granulomas present, changes
suggestive of hemophagocytosis. He was given high dose dexamethasone and etoposide. His LRTs began to
improve. After tolerating 2 doses of etoposide, he was discharged home with follow up.
The hemophagocytic or hemophagocytic lymphohistiocytosis (HLH) is a syndrome encompassing a heterogeneous
group of disorders characterized by persistent activation of benign macrophages, leading to uncontrolled secretion of
cytokines and phagocytosis of blood cells. The syndrome can be primary due to mutations in different genes involved
in lymphocyte cytotoxicity and secondary in association with infectious, autoimmune, or malignant disorders. HLH is
characterized by fever, hepatosplenomegaly, cytopenias, hypertriglyceridemia.Hepatosplenomegaly is a hallmark of
HLH. The diagnosis is based on a constellation of clinical, laboratory, and histological fnding. Two forms of HLH are
recognized: a primary familial form and a secondary hemophagocytic syndrome. Primary HLH is often triggered by
infection, making the distinction between primary and secondary forms difficult. Hepatic manifestations are seen in
nearly all patients with HLH and they may range from mild synthetic dysfunction to overt hepatic failure. In HLH the
iron is deposited in the spleen and bone marrow. Liver damage, regardless of the cause, can result in the release of
large amounts of iron in the form of ferritin.
HLH should be considered in the differential diagnosis of liver failure, especially if accompanied by cytopenias and
prolonged fever. It is crucial to have awareness of clinical symptoms and diagnostic criteria in order not to overlook
HLH and to start life-saving therapy in time.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: Yes
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Ghulamullah Shahzad : ACG Member
Sumair Akhtar : ACG Non-Member
Prakash Viswanathan : ACG Member
Kaleem Rizvon : ACG Member
Paul Mustacchia : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: [No
Comments]
CONTROL ID: 1745252
TITLE: Primary hepatic hodgkin’s lymphoma (HL) masquerading as drug induced liver injury (DILI)
PRESENTER: Angela Hira
PRESENTER (INSTITUTION ONLY): UMDNJ-RWJMS
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: 76-year-old man, with history of diabetes mellitus, hypertension, and hyperlipidemia presented at an outside
hospital with three days of acute onset right and left upper abdominal pain and fever. He also reported ten pound
weight loss over the last eight months. He was compliant with all his medications, metformin, glimperide, simvastatin,
ramipril, nebivolol. Physical examination was significant for scleral icterus, mild tenderness in the right and left upper
quadrants, enlarged liver that was firm but non-tender and 4cm below the right costal margin. No lymphadenopathy
was palpated. Initial labs: total bilirubin 10.5 (0.3-1.2 mg/dl), indirect bilirubin 8.4 (0-0.45 mg/dl), alkaline phosphotase
305 (42-133 IU/l), SGOT 283 (15-41 IU/l), SGPT 181(7-40 u/l), Hgb 13.1 (14-18 g/dl), WBC 8.3 (4.8-10.8 thou/cmm),
PLTS 62 (130-400 tho/cmm) and INR 1.37. All laboratory data from one month prior was normal. CT scan of abdomen
and pelvis revealed cholelithiasis, hepatomegaly and heterogenous lesions in an enlarged spleen; MRCP did not
show choledocholithiasis. Hepatitis A, B and C, HIV, CMV, EBV, ANA, smooth muscle antibody, ceruplasmin,
hemochromatosis gene analysis, anti-mitochondrial antibody CA19-9 and CEA were all negative. Initial liver biopsy
report suggested DILI and a second pathology opinion was requested. All hepatotoxic medications were
discontinued. His clinical status was stable but no improvement in his LFTs for the next 20 days. He then presented
with slurred speech and right-sided weakness due to acute/subacute infarct of left middle cerebral artery. There was
no improvement in his liver tests at this admission. The liver biopsy second opinion reported expanded portal tracts
with predominantly lymphocytic infiltrate and histocytes. Large atypical cells with irregular nuclear contours and
prominent nucleoli were noted to be CD30, PAX5 and CD20 positive and negative for CD15, CD45, and ALK. These
findings are consistent with HL.
In view of the HL chemotherapy complication risks and the continued clinical deterioration, patient’s family decided to
transition care to hospice. HL has a bimodal presentation with second peak at >55. Most patients with HL develop
hepatic complications late in the disease course and have other extra-hepatic HL involvement. Our case represents
the rare occurrence of primary HL of the liver, which was initially attributed to DILI. The elderly are at the greatest risk
of DILI due to factors such as poly-pharmacy, co-morbidities and nutritional status but it important to consider other
etiologies.
Methods: NA
Results: NA
Conclusion: NA
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Angela Hira : ACG Non-Member
Anita Cheruvanky : ACG Non-Member
Jill Collier : ACG Member
Sita Chokhavatia : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: [No
Comments]
CONTROL ID: 1745434
TITLE: Rare Case of Rituximab associated Hepatitis B Virus Reactivation With Co-existence of IgM Anti-hepatitis A
and IgM Anti-hepatitis E Antibodies
PRESENTER: Shehzad Merwat
PRESENTER (INSTITUTION ONLY): The University of Texas Medical Branch
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 68 year old Caucasian man was seen in hospital for abnormal LFTs. He carried a diagnosis of HHV-8
related plasmablastic T-cell lymphoma. He had undergone treatment with cyclosporine, doxorubicin, vincristine, and
prednisone with initial remission of disease; however, he developed recurrence and was subsequently treated with
rituximab 8 months prior to presentation. Before the initiation of chemotherapy, the patient underwent testing for
Hepatitis B (HBV), which demonstrated he was HBV surface antigen (HBsAg) negative, anti-HBV surface antibody
(anti-HBS) positive, and IgM anti-HBV core antibody (anti-HBc IgM) negative. A total anti-HBV core antibody (anti-HBc
total) was not checked prior to starting therapy. On the current admission, total bilirubin was 7.9 mg/dL with
conjugated fraction of 4.7 mg/dL. AST was elevated to 830 U/L, ALT to 1591 U/L, and alkaline phosphatase to 189
U/L. Serum ANA was positive at a titer of <1:80 and anti-smooth muscle antibody was negative. Ceruloplasmin was
noted at 44 mg/dL. Serologies demonstrated HBsAg to be positive, anti-HBs negative, anti-HBc total positive, antiHBc IgM positive, HBeAg positive, and anti-HBe negative. HBV PCR found 5.81 Log IU viral particles. Furthermore,
his hepatitis A virus (HAV) total antibody was positive and anti-HAV IgM antibody was reactive. His anti-Hepatitis E
virus (HEV) IgM antibody was also detected, and anti-HEV IgG was negative. Hepatitis D antibody was negative. Liver
biopsy showed irregular hepatic plates with hepatocyte dropout, peri-portal inflammation, multiple apoptotic bodies
and ballooning degeneration. Stage 1 to 2 fibrosis was found. Tenofovir 300mg daily was started for reactivated HBV
and his AST, ALT, and bilirubin declined to normal 16 weeks later. Acute hepatitis resulting from co-infection with
multiple hepatotropic viruses may occur. In some instances the mechanism by which they are contracted and risk
factors for their exposure are shared. In the developing world, several case reports and series have described
instances where patients presented with serologic evidence for acute infection from both HAV and HEV. These
studies have generally been performed in the setting of sporadic cases with clinical syndromes of acute hepatitis.
However, the use of serologic testing to establish diagnoses of acute HAV or HEV in these settings is problematic.
Serologic tests were designed for cases in which the pretest probability and clinical suspicion for exposure to acute
HEV or HAV were high (i.e., epidemic outbreaks or travel to endemic areas). Whether the presence of anti-HAV and
HEV in the setting of such sporadic cases are indicative of true co-infection or represent false positive results remains
debatable.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Sheharyar Merwat : ACG Non-Member
Shehzad Merwat : ACG Member
Andrea Duchini : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: [No
Comments]
CONTROL ID: 1745553
TITLE: Idiopathic Hyperammonemia following Rituximab for Rheumatoid Arthritis
PRESENTER: Randhir Jesudoss
PRESENTER (INSTITUTION ONLY): Christ Hospital
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction
Idiopathic Hyperammonemia (IHA) is a syndrome of neurological changes with unexplained and often marked
elevations in serum ammonia. We report a case of Idiopathic Hyperammonemia in a 53 year old woman following
rituximab use as a disease modifying drug (DMARD) for rheumatoid arthritis.
Case Presentation
53 year old woman presented with somnolence and involuntary movements of her extremities for one week. There
was no history of fevers, jaundice or abdominal pain. She had severe steroid dependent rheumatoid arthritis failing
several DMARD`s. Most recent therapies included Rituximab, Leflunomide and Methotrexate. Physical exam findings
included lethargy, fine tremor, myoclonic jerks and joint swelling.
Labs showed an initial serum ammonia level of 472 g/dl with normal liver function tests and creatinine. Viral
serologies and imaging to rule out portal vein thrombosis were negative. A liver biopsy showed mixed micro vesicular
and macro vesicular steatosis with no evidence of inflammation. Plasma and urine amino acid metabolite profile was
negative for any occult urea cycle disorders, fatty acid oxidation defects and branched chain aminoaciduria.
Lactulose, Rifaximin and sodium phenyl acetate plus sodium benzoate failed to improve her ammonia levels. Protein
restriction and dietary formula containing only branched chain amino acids were instituted to promote reduced muscle
breakdown .Consistent control of her ammonia levels was achieved only with daily hemodialysis. Without HD, her
serum ammonia levels rose to as high as 798 g/dl and mental status worsened requiring mechanical ventilation. She
succumbed after a month of supportive care.
Discussion
The diagnosis of Idiopathic Hyperammonemia is a diagnosis of exclusion; with acute onset of encephalopathy
associated with elevated serum ammonia, with no hepatic dysfunction In our patient, all other causes of
hyperammonemia were systematically excluded as detailed above. Isolated reports of IHA with rituximab based
chemotherapy regimens have been reported. However, Hyperammonemic encephalopathy has not been previously
reported with use of rituximab as a DMARD; this is interesting to note because the usual doses needed to treat
rheumatoid arthritis are considerably lower than those used to treat malignancies. The probable cause as described in
case series have been acquired urea cycle defect as the cause of hyperammonemia. Physicians should consider IHA
in the differential of altered mental status in patients receiving rituximab as earlier recognition and institution of early
CVVHD has been reported to reduce mortality
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: Yes
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Randhir Jesudoss : ACG Non-Member
Sarat Chandra : ACG Non-Member
Deepika Appalla : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: [No
Comments]
CONTROL ID: 1745660
TITLE: What’s All the Pus About? An Unusual Cause of Fever in a Cirrhotic Patient
PRESENTER: Tyrone Robinson
PRESENTER (INSTITUTION ONLY): Walter-Reed National Military Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Refractory hepatic hydrothorax is a common finding in decompensated cirrhosis. One of the complications of
this process includes infection of the pleural fluid also known as spontaneous bacterial empyema (SBEM). We
describe the case of an 83-year-old male with hepatitis B associated cirrhosis with refractory hepatic hydrothorax who
developed SBEM. This case describes risk factors, diagnosis, pathophysiology and management of this challenging
complication.
An 83-year-old man with decompensated, HBeAg positive hepatitis B associated cirrhosis and history of refractory
hepatic hydrothorax who was recently started on entecavir presented with acute onset fever, dyspnea and diffuse
abdominal pain. Medications included spironolactone, furosemide and aspirin. Exam was notable for BP 93/57, HR
108/min, RR 28 and SaO2 96% on 4L 02, icteric sclera, decreased breath sounds and dullness to percussion of the
right hemithorax, abdomen distention with shifting dullness and no asterixis. Labs revealed a leukocytosis with 25%
bands, a stable macrocytic anemia, thrombocytopenia, coagulopathy, mildly elevated hepatocellular enzymes, and an
acute kidney injury. CXR confirmed right pleural effusion and RUQ ultrasound revealed large volume ascites.
Thoracentesis was performed and yielded WBC 429, PMN 81%, LDH 103, protein <2 g/dL and culture of this fluid
grew Escherichia coli consistent with SBEM. Ceftriaxone and albumin were administered resulting in sterilization of
the pleural fluid.
Diagnostic criteria for SBEM includes positive pleural fluid culture or a pleural fluid PMN count greater than 500
cells/mm3, no evidence of pneumonia and preexisting hepatic hydrothorax. Although 10% of cirrhotic patients with
ascites have associated pleural effusion only 13% of these patients develop SBEM. Pathogenesis may arise from
penetration of infected ascitic fluid into the pleural cavity through the diaphragm, or, as is likely in our case through
bacteremia with seeding of E. coli in the pleural fluid, which commonly occurs in portal hypertension. Mortality
associated with SBEM is reported to be as high as 20% with poor prognostic factors including ICU admission, high
MELD-Na score, and initial antibiotic treatment failure. Prompt therapy with 3rd-generation cephalosporins or a
carbapenem are key in decreasing mortality. Factors associated with development of SBEM include SBP, a high
Child-Pugh score and low pleural fluid protein. Given the nonspecific nature of symptoms a high index of suspicion is
required for the diagnosis of SBEM and a diagnostic thoracentesis should be carried out in patients with hepatic
hydrothorax presenting with fever, pain, encephalopathy, or unexplained deterioration in renal function.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Tyrone Robinson : ACG Non-Member
Ryan Kwok : ACG Member
John Bassett : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: [No
Comments]
CONTROL ID: 1745735
TITLE: EndoHepatology : overlap of endoscopic procedures within the practice of Hepatology
PRESENTER: Susana Lopes
PRESENTER (INSTITUTION ONLY): H.S.João
PRESENTER (COUNTRY ONLY): Portugal
ABSTRACT BODY:
Purpose: A 77 years old male, with subtotal gastrectomy performed in 2010 for gastric GIST treatment, was admitted
in ER with melenae in December 2011. Upper endoscopy showed a subepithelial mass with mucosal ulceration and
na oozing visible vessel. Hemostasis was achieved with adrenaline injection and hemoclipping. CT scan revealed an 8
cm gastric tumor, interpreted as GIST recurrence. At the same time, 2 nodular lesions in the left hepatic lobe were
identified, with 2 and 3cm, described as liver metastasis.
Endoscopic ultrasound (EUS) with Fine Needle Aspiration (FNA) of both gastric and liver lesions was performed.
Histology and immunohistochemistry confirmed a GIST tumor in the stomach, but revealed a hepatocellular carcinoma
in the liver.
Patient was submitted to gastrectomy and left hepatectomy, with confirmation of the EUS FNA findings.
Conclusion: Liver biopsy is an emerging application of EUS in patients with focal liver lesions.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Susana Lopes : ACG Member
João Antunes : ACG Non-Member
Joanne Lopes : ACG Non-Member
Guilherme Macedo : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: [No
Comments]
CONTROL ID: 1745796
TITLE: Secondary hepatocellular carcinoma following hepatic infiltration of chronic lymphocytic leukemia
PRESENTER: Chika Ezigbo
PRESENTER (INSTITUTION ONLY): Metropolitan Hospital/New York Medical College
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: 75 year old Hispanic female, from Puerto Rico, who presented to our hospital in 2008 for oncology
evaluation. She had been diagnosed of Chronic lymphocytic leukemia(CLL) four months earlier. This was confirmed
by a sternal bone marrow aspiration and. At that time she was completely asymptomatic and had no palpable
lymphadenopathy. Other pertinent past medical history were diabetes mellitus, hypertension, hyperlipidemia and
migraine headaches. Laboratory exams were notable for mild lymphocytosis. Flow cytometry showed typical CLL with
CD 19+/CD5+ (co-expression), CD20+ (dim), CD23+, CD38- and kappa light chain+ (dim), 0% of ZAP 70 positive.
Bone marrow cytogenetics showed normal karyotype.
Since her presentation, she had an abnormal elevation in alkaline phosphatase that ranged from 288U/L to 440U/L.
Hepatitis C antibody and Hepatitis B surface antigen were negative. All work up for chronic liver disease were
negative. She underwent a liver biopsy which showed liver parenchyma with a patchy infiltrate of small lymphocytes
expressing CD20, PAX-5,CD5,CD23,CD43, and BCL-2 characteristic of B-small lymphocytic lymphoma/Chronic
lymphocytic leukemia. Serial CT scans showed progressive intra-abdominal lymph node affectation, however she did
not meet criteria for treatment for her CLL as her WBC count as well as other markers of disease activity remained
stable
In 2012, as part of the routine evaluation of her progressive intra-abdominal lymphadenopathy, an abdominal CT scan
showed an 8cm liver mass. Though initially asymptomatic, she developed a right upper quadrant pain that was
severe, associated with malaise, constipation and loss of appetite. Physical examination showed submandibular
lymphadenopathy, and right upper quadrant tenderness. She had no peripheral stigmata of chronic liver disease. The
presence of a large liver mass with an underlying history of liver biopsy being positive for CLL/B-lymphocytic
lymphoma made a suspicion of a rapidly growing lymphoma likely. Alpha fetoprotein was also normal. She underwent
a second liver biopsy that now revealed Grade II Hepatocellular carcinoma (HCC).
Being Child Pugh Stage B, with a huge liver mass and maintaining a good functional status, she only met the
Barcelona Clinic Liver Cancer (BCLC) criteria for treatment with sorafenib which she was started on but tolerated for
only few weeks. Unfortunately, she continued to decline while the tumor increased exponentially. She was eventually
placed in a hospice and died three weeks later.
There may be a real association between HCC and CLL. Future studies are required to establish evidence and the
goals of treatment.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Chika Ezigbo : ACG Non-Member
Nora Bergasa : ACG Non-Member
Noella Boma : ACG Non-Member
IMAGE CAPTION:
(no table selected)
AVERAGE SCORE: 4.5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: [No
Comments]
CONTROL ID: 1745885
TITLE: A blistering case of Hereditary Hemochromatosis
PRESENTER: Thomas Coppola
PRESENTER (INSTITUTION ONLY): Winthrop University Hospital-Department of Internal Medicine
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Case Presentation: 59 year old male with history of psoriasis and moderate alcohol use presents with
blistering of the skin. Biopsies revealed subepidermal bulla. Serum porphyrins were ordered to evaluate for Porphyria
Cutanea Tarda (PCT). Total Porphyrins were high 29.1, predominantly Uroporphyrin 13.6 consistent with PCT. Patient
was also found to have elevated liver related tests ALT 79, AST 53 and serum ferritin of 715. He was referred for
further evaluation and he was found to have elevated transferrin saturation. Genetic testing revealed he was
homozygous for the C282Y HFE mutation consistent with hereditary hemochromatosis.
Literature Review: Hereditary Hemochromatosis (HH) is the most common-identified- genetic mutation in Caucasians
with a prevalence of approximately 1 per 220-250 individuals of northern european origin. The pathophysiologic
predisposition to increased inappropriate absorption of dietary iron may lead to development of life-threatening
complications of cirrhosis, hepatocellular carcinoma, diabetes and cardiac disease. Genetic research has led to the
discovery of the HFE gene, most notably the C282Y mutation causing hereditary hemochromotosis. A genetic
diagnosis can be applied to individuals who have not yet developed any phenotypic expression. These individuals
have a genetic susceptibility to develop iron overload, but may or may not do so to a variable degree.
Clinical Significance: In this case, the patient presented with a clinical syndrome, (PCT) which, pathophysioligically
has been associated with elevated iron stores. Notably, the patient had a history of being a frequent blood donor,
keeping iron levels from rising for most of his life. Mild liver related lab abnormalities at the time of diagnosis of PCT,
led to a clinical suspicion of HH.
Research Questions: Will early detection of a genetic mutation assist in prevention of complications from this disease?
How does PCT relate to HH?
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Thomas Coppola : ACG Member
Vineet Korrapati : ACG Member
Peter Malet : ACG Member
James Grendell : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: [No
Comments]
CONTROL ID: 1745974
TITLE: Thorotrast Induced Chronic Liver Disease - A Rare Finding in Today's Clinical Practice
PRESENTER: Ibrahim Habib
PRESENTER (INSTITUTION ONLY): Advocate Lutheran General Hospital
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: We present the case of an 83 year-old female who presented with recurrent ascites and chronic liver
disease of uncertain etiology. Paracentesis revealed fluid with a SAAG > 1.1, suggestive of portal hypertension. Liver
workup, including autoimmune labs, viral hepatitis serologies, and iron studies, was unremarkable. Additional labwork
was significant for thrombocytopenia and a normal CEA. Medical history was negative for alcohol abuse, diabetes,
and obesity. Liver ultrasound with doppler was normal with no evidence of thrombosis, focal intrahepatic
abnormalities, or biliary duct dilatation. CT of the abdomen with contrast demonstrated a cirrhotic appearing liver
along with prominent, contrast-enhancing high density material within the spleen and peripancreatic lymph nodes.
Transjugular liver biopsy demonstrated periportal fibrosis along with focal granular foreign body material. Upon further
inquiry, it was elucidated that the patient had received thorotrast for imaging of a cirosoidal aneurysm in the 1950s.
Thorotrast, a radioactive suspension containing thorium dioxide, was used as a contrast agent in the United States up
until the late 1950s. Thorotrast offered high image quality and, at that time, no immediate side effects were noted. As
was the case in our patient, it was primarly used for cerebral angiography. Worldwide, approximately 100,000 people
were exposed to thorotrast from 1930 to 1964. Subsequently, it was discovered that thorotrast induced liver disease
and tumors decades after its use. Our case is unique in that thorotrast-induced chronic liver disease is seldom seen
in modern-day clinical practice.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Ibrahim Habib : ACG Non-Member
Peter Sargon : ACG Member
Baseer Qazi : ACG Member
Thorotrast induced enhancement of spleen. Ascites also present.
IMAGE CAPTION: Thorotrast induced enhancement of spleen. Ascites also present.
(no table selected)
AVERAGE SCORE: 3.5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: [No
Comments]
CONTROL ID: 1745982
TITLE: Rupture of Visceral Artery Aneurysms in a Patient With Sjogren’s Syndrome
PRESENTER: Kaartik Soota
PRESENTER (INSTITUTION ONLY): Unity Health System
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Visceral artery aneurysms are very rare. Among these hepatic artery aneurysms (HAA) are 2nd most
common with an incidence of 20% while Gastro-duodenal artery aneurysms (GDAA) are even rarer with an incidence
of less than 10% of all such lesions. We report the rupture of these aneurysms in a patient of Sjogren’s syndrome
(SS).
Case
A 69 year old female with history of SS and hypertension presented to the emergency department with abdominal pain
and blood in stools for 2 days. On physical examination, she had a HR of 129, with a very tense and diffusely tender
abdomen without any bowel sounds. Blood work showed hemoglobin of 11.4 gm/dl which dropped to 8.0 gm/dl in 6
hrs. Abdominal CT scan showed large intra-abdominal hematoma, pelvic ascites and aneurysm of the common
hepatic artery (figure). Subsequent arteriography revealed an HAA along with a GDAA without any active bleeding.
Both of them were embolized with coils. Her Hb stabilized, repeat CT scan 6 days later showed stable hematoma and
she was discharged home.
Discussion
Visceral artery aneurysms are usually associated with atherosclerosis but can also occur with mycotic infections and
vasculitis. They have a high mortality rate of 21% and rupture is most often the initial presentation. The classic triad
consists of abdominal pain, jaundice and gastro-intestinal hemorrhage. Arteriography is the gold standard for
diagnosis and the treatment is either surgical or endovascular repair. Our patient had SS which is known to cause
small and medium vessel vasculitis. She also had a remote history of intra-cranial bleed due to aneurysmal rupture
which has been reported in SS. Of note, she did not have any abdominal artery aneurysm which is expected in a
patient with atherosclerosis but not with SS. Hence, we believe that she had these aneurysms secondary to her SS.
Conclusion
Visceral artery aneurysms carry a high mortality rate if not readily diagnosed and treated. Most of them are due to
atherosclerosis and their association with vasculitis is rare. In our literature search this is the first reported case of
such aneurysms in SS.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: Yes
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Kaartik Soota : ACG Non-Member
Anup Singh : ACG Non-Member
Ziad Alkhoury : ACG Non-Member
Manuel Matos : ACG Non-Member
Figure 1
IMAGE CAPTION: Figure 1
(no table selected)
AVERAGE SCORE: 2.5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: Mayo
Clin Proc. 1995 Jun
70(6):565-9.
Rheumatoid vasculitis manifesting as intra-abdominal hemorrhage.
Achkar AA, Stanson AW, Johnson CM, Srivatsa SS, Dale LC, Weyand CM.
Source
Division of Rheumatology and Internal Medicine, Mayo Clinic Rochester, Minnesota 55905, USA.
CONTROL ID: 1746159
TITLE: Superior Mesenteric Vein to Right Gonadal Vein Portosystemic Shunt Resulting in Hemorrhage from Duodenal
Varices in a Cirrhotic
PRESENTER: Abdillahi Abdinoor
PRESENTER (INSTITUTION ONLY): Loyola University Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Background: Portal hypertension in patients with end stage liver disease can lead to the development of
varices. While they are most commonly identified in the esophagus or stomach, ectopic small bowel varices also
occur. Hemorrhaging of duodenal varices is a rare but reported cause of GI bleeding, occurring in <5% of cirrhotics.
Prompt diagnosis is required as these patients have mortality rates >40-50%. Treatment includes endoscopic ligation
or sclerotherapy, interventional radiology procedures, or surgical intervention.
Case Report: A 35 year-old woman with alcoholic cirrhosis was transferred from an outside hospital with
hematemesis, melena, and abdominal pain. She had upper/lower endoscopy, which revealed isolated non-bleeding
duodenal varices and portal hypertensive gastropathy. Though no bleeding was seen, she had ongoing melena and
required >15 units of blood during her one week hospitalization there.
She was transferred to our institution with a hemoglobin of 9.1 but continued to have melena and within 6 hours of
admission, had a 3 gram hemoglobin drop. CT showed no portal or splenic vein thrombosis but confirmed the
presence of duodenal varices. Subsequent endoscopy showed isolated, large, non-bleeding varices in the 1st and 2nd
part of the duodenum. TIPS was performed across the left hepatic vein to the portal vein with subsequent reduction in
the hepatic vein pressure gradient from 20 to 4 mm Hg. During the procedure, superior mesenteric vein varices were
seen with drainage into the right gonadal vein which accounted for the presence of isolated duodenal varices. She
underwent embolization of these varices, and her hemoglobin remained stable thereafter.
Conclusion: Portosystemic shunting can occur in unusual locations leading to atypical location of varices and
hemorrhaging in the cirrhotic with high morbidity and mortality if not quickly identified. While no guidelines exist on
management of these varices, treatment ultimately requires a multidisciplinary approach.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Abdillahi Abdinoor : ACG Member
Priya Kathpalia : ACG Member
Aditya Dholakia : ACG Member
A. Samad Soudagar : ACG Member
Marc Borge : ACG Non-Member
Eric Kallwitz : ACG Non-Member
Direct portal venography during TIPS demonstrates hepatofugal flow in the SMV with a dense network of duodenal
varices (arrow). PV-portal vein, GV-gonadal vein.
IMAGE CAPTION: Direct portal venography during TIPS demonstrates hepatofugal flow in the SMV with a dense
network of duodenal varices (arrow). PV-portal vein, GV-gonadal vein.
(no table selected)
AVERAGE SCORE: 4
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: [No
Comments]
CONTROL ID: 1746181
TITLE: Amoxicillin-Induced Hepatotoxicity
PRESENTER: Aquanette Brown
PRESENTER (INSTITUTION ONLY): Georgetown University Hospital
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: INTRODUCTION
Amoxicillin is a frequently prescribed antibiotic. Amoxicillin-clavulanate (especially clavulanic acid) has the rare
potential to cause a cholestatic hepatitis. However, amoxicillin’s alone risk of causing hepatic cholestasis and hepatitis
is less well recognized. Here, we present a case of a hepatotoxicity in a woman who received amoxicillin after a
dental procedure.
CASE REPORT
A 45 yr old female presented with pruritus and jaundice and was found to have elevated liver enzymes (LFT). No h/o
of any liver disease. The patient reported completing a five day course of amoxicillin 875mg by mouth twice per day
after wisdom teeth removal 35 days prior to admission. Her renal function, complete blood count were normal.
Toxicology screening was negative. Her LFTs were normal two months prior to admission. Anti-mitochondrial
antibody (AMA), antinuclear antibody, anti-smooth muscle antibody, liver kidney microsomal Type 1 antibody, hepatitis
A IgM antibody, hepatitis B surface antigen, hepatitis B core total antibody, hepatitis C antibody, HCV RNA PCR
quantitive and hepatitis E IgM antibody were all negative or undetectable. Past medical history included non-smallcell lung carcinoma status post left lobectomy, uterine fibroid removal, and hypertension. Family history was negative
for any liver disease.
Hepatobiliary iminodiacetic acid scan showed poor uptake of the isotope consistent with an acute hepatitis. Repeat
ultrasound showed a normal appearing liver parenchyma, and bile ducts and a contracted gallbladder with
adenomyomatosis, and no evidence of acute cholecystitis. Endoscopic retrograde cholangiopancreatography was
normal. MRI of the abdomen without contrast showed mild irregularity of the intrahepatic biliary ducts concerning for
inflammatory cholangiopathy, no abnormalities of the extrahepatic duct, no specific features of adenomyomatosis,
normal liver morphology, and a few pancreatic cysts. Liver biopsy showed prominent cholestasis, periductal
cholangitis and fibrosis. Portal triaditis with eosinophils was present. There was no evidence of granulomas,
autoimmune hepatitis, or malignancy. Patient was started on cholestyramine for her pruritus and ursodiol 300mg by
mouth twice per day for the drug induced cholestasis until her LFTs improved significantly (AST-18, ALT-19, TB-0.7,
AP- 194) after few weeks of conservative treatment.
DISCUSSION:
Amoxicillin-induced liver injury increases when patients use it with clavulanate. A correct diagnosis of drug induced
liver injury may prevent more expensive and extensive diagnostic testing/procedures for a patient.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Aquanette Brown : ACG Non-Member
Manie Juneja : ACG Non-Member
Jacqueline Laurin : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 5.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: [No
Comments]
CONTROL ID: 1746216
TITLE: An Unusual Presentation of Auto-immune Hepatitis
PRESENTER: Mark Salem
PRESENTER (INSTITUTION ONLY): Los Angeles County + University of Southern California Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: 26-year-old Caucasian male with no significant history presented with new onset jaundice for 3 weeks. Two
weeks prior to admission, he developed daily nausea and vomiting. One week prior to admission he developed night
sweats, anorexia, constipation, and generalized pruritis. In addition he began to experience a post-prandial right
upper quadrant abdominal pain with no radiation and a 16 pound weight loss which prompted presentation to the
hospital. His medications included occasional acetaminophen/ diphenydramine PRN for insomnia. Family history was
significant for cholelithiasis in his mother and lung cancer in multiple family members. Patient’s social history included
consumption of approximately 5oz of spirits per week, a remote tobacco history, experimentation with intravenous
heroin as well as multiple professionally obtained tattoos.
Pertinent physical exam findings included stable vital signs, icterus, a soft and nontender abdomen with liver edge
palpated 2cm below the costal margin and percussed splenomegaly. No lymphadenopathy or asterixis were
appreciated. Laboratory findings were significant for AST of 825 U/L, ALT of 596 U/L, total bilirubin of 26 mg/dL with a
direct bilirubin of 20 mg/DL and alkaline phosphatase of 118 U/L. His INR was 1.46 with a PT of 17.4, albumin of 3.1
g/dl and total protein of 6.8 g/dl. Abdominal ultrasound revealed a nodular liver surface, hepatosplenomegaly, marked
gallbladder thickening, and enlarged peripancreatic lymph nodes consistent with acute hepatitis. Hepatitis A,B & C
serologies were negative. His ferritin was 423 ng/mL with a % saturation of 38. Anti-mitochondrial antibody, anti-LKM
and alpha 1 anti-trypsin titers were within normal limits. His total IgG was 2657 (reference range 650-1600.) Anti
smooth muscle antibody titers were measured at 36U (reference range <20.)Given his clinical picture along with an
International Autoimmune hepatitis group scoring was10, treatment was started for autoimmune hepatitis with
corticosteroids. His clinical picture improved soon thereafter.
Discussion: This case represents an unusual presentation of autoimmune hepatitis Autoimmune hepatitis is typically
diagnosed in the fourth or fifth decade of life and more commonly affects females. It typically presents with markedly
elevated ASTs compared to bilirubin and alkaline phosphatase, as was seen in this case. This presentation
demonstrates, however, that this condition can present at any age and also affect males. Autoimmune hepatitis
should, therefore, remain high on the differential in young males with hepatitis.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Mark Salem : ACG Non-Member
Haig Aharonian : ACG Non-Member
Takeshi Saito : ACG Non-Member
Anisa Shaker : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: ANA
not included?
CONTROL ID: 1746319
TITLE: Acute fatal presentation of adult onset Ornithine Transcarbamylase (OTC) Deficiency
PRESENTER: Rahul Nayani
PRESENTER (INSTITUTION ONLY): University of Missouri
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 19 year soldier was admitted to ICU from an outside hospital with seizures. He was admitted there with
altered mental status 3 days prior. An extensive work up for infectious and toxic etiologies was negative at the time.
He improved on empiric antibiotics and was discharged with a diagnosis of encephalopathy of unknown etiology. He
was readmitted and transferred to our hospital with status epilepticus. History was negative for preceding viral
prodrome, aspirin and recreational drug use, travel history or insect bites. His developmental and family history was
unremarkable and was only taking multivitamins. At admission, he was found to have fever of 38.3 with tachycardia
and normal blood pressure. Examination was significant for mild hepatomegaly with no signs of advanced liver
disease. Neurological examination was non focal with bilateral down-going planters and negative meningism. He was
started on propofol, fosphenytoin and levetiracetam with control of seizures. His comprehensive metabolic profile was
significant for elevated creatinine at 1.88, elevated AST and ALT at 88 and 189 IU/ml with normal bilirubin, alkaline
phosphatase and synthetic functions. Ammonia level was significantly elevated at 1248 mmol/L. Other work up
including acute hepatitis panel, iron studies, ANA and serum ceruloplasmin were normal. CT head showed bilateral
diffuse sulcal effacement. USG abdomen showed decreased parenchymal echogenicity. Lumbar puncture and a
metabolic drug screen were normal. Patient was started on hemodialysis along with IV infusions of ammonul, arginine
& empiric levocarnitine with improvement of NH3 down to 112 by the next day. Acylcarnitine profile, Urine Amino
Acids, Urine Orotic Acid levels and OTC Comprehensive Sequence & Deletion Duplication Analysis were sent out.
However, despite being off sedation, he displayed no signs of spontaneous neurological activity and was declared
brain dead after two formal assessments. His Urine Orotic Acid level came back elevated at 225.9 mmol/mol and his
DNA analysis revealed R277W mutation at exon 8 for OTC gene.
OTC deficiency is the most common enzyme deficiency for urea cycle disorder. Being an X linked pattern of
inheritance, it most commonly affects males in infancy with a wide range of clinical presentations. With more than 40
point mutations and nucleotide deletions described for the OTC gene, it has variable phenotypical presentations with
variable severity and outcomes. Our case is unique presentation at a later age which is rare and emphasize the
importance of considering as differential in any patient with altered mental status irrespective of age as prompt and
early diagnosis has the potential to prevent lethal outcomes.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Rahul Nayani : ACG Non-Member
Sameer Siddique : ACG Member
Murtaza Arif : ACG Member
Hazem Hammad : ACG Member
Matthew Bechtold : ACG Member
Jamal Ibdah : ACG Member
Abhishek Choudhary : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: [No
Comments]
CONTROL ID: 1746418
TITLE: Coincident Autoimmune Hepatitis, Hepatitis C And Celiac Disease In A Young Patient With Decompensated
Cirrhosis
PRESENTER: Alvaro Toledo
PRESENTER (INSTITUTION ONLY): Geisinger Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 28 year old female with hypothyroidism from Grave’s disease and narcotic dependence was seen in the
liver clinic for cirrhosis and chronic hepatitis C. The patient had variceal bleeding 2 months treated with endoscopic
banding. The patient likely contracted hepatitis C through IV drug use 5 years before the diagnosis. The ANA was
positive at 1:320, anti-smooth muscle antibody elevated at 39.2 u (normal <20), and hypergammaglobulinemia was
present (2.4g/ml). Hepatitis C was genotype 1, viral load 142,918 IU/ml. Initial liver chemistry revealed alkaline
phosphatase 235, AST 98, ALT 118, total bilirubin 0.4, and INR 1.2. Platelet count was 87,000. Liver biopsy showed
cirrhosis with mixed inflammation with lymphocytes and plasma cells, consistent with hepatitis C with co-existing
autoimmune hepatitis. CT scan showed a cirrhotic liver, portal hypertension, and extensive mesenteric adenopathy.
EGD/EUS revealed benign lymph nodes but scalloped mucosa in the duodenum; pathology showed blunting of villi
and increased intraepithelial lymphocytes in lamina propia consistent with celiac disease. Tissue transglutaminase
(TTG) was greater than 167 units. The patient was counseled about a gluten free diet but was not compliant with it.
Repeat TTG levels have not improved. For autimmune hepatitis, low dose azathioprine (25-50mg daily) was begun
with initial normalization of AST and ALT. However, had to be stopped within a year due to severe anemia. Because
of untreated autoimmune hepatitis, relatively advanced cirrhosis, noncompliance, and poor social support, we were
not able to treat hepatitis C. During followup over the next three years, the patient complained of unintentional weight
loss, easy fatigability, diarrhea and intermittent right upper quadrant abdominal pain. She continues to have local
hospital admissions requiring blood transfusions. She was last admitted in our hospital in December 2012 (age 30) for
hematemesis and melena with hemoglobin of 6g/ml. EGD showed grade II varices which were banded. The day after
endoscopic banding, she left the hospital against medical advice, and is currently incarcerated. We believe that the
early and severe cirrhosis in this case was likely caused by a combination of autoimmune and viral hepatitis.
Uncontrolled celiac disease might also have contributed. For hepatitis C, autoimmune hepatitis, and celiac disease,
there are multiple case reports of 2 of 3 of these entities co-existing. This is the first report of all three disease entities
co-existing in one patient. This complicated liver disease, worsened by a difficult social situation, has made clinical
managment particularly challenging.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: Yes
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Alvaro Toledo : ACG Non-Member
Chuan Miao : ACG Non-Member
David Diehl : ACG Member
Jinhong Li : ACG Non-Member
Robert Smith : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Haritha Avula: [No Comments]|James Buxbaum: [No Comments]|Raquel Davila: [No Comments]|Brian Weston: [No
Comments]
CONTROL ID: 1746463
TITLE: Common Variable Immunodeficiency causing Non Cirrhotic Portal Hypertension:Case report and a Review of
Literature
PRESENTER: Jean Ong Kian Koc
PRESENTER (INSTITUTION ONLY): Einstein Medical Center - Gastroenterology
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Common variable immunodeficiency (CVID) is marked by a deficiency of immunoglobulins due to impaired B
cell differentiation. Patients manifest with recurrent bacterial infections and are often diagnosed as young adults. We
present a case of a 57 yo male with CVID who was previously well until 4 weeks prior to consultation when he noticed
ascites and bipedal edema. Hemogram was remarkable for thrombocytopenia (98), all other cell lines were normal.
Renal, cardiovascular work-up and synthetic function were unremarkable. However, alkaline phosphatase ( 183 IU/L )
and liver transaminases were elevated ( AST 56 IU/L ; ALT 62 IU/L ). Hepatitis serologies and autoimmune markers
were all negative. MRI imaging revealed nodular contour of the liver , splenomegaly , patent portal and hepatic veins
and portosystemic venous collaterals. Large esophageal varices were found on endoscopy and variceal ligation with
banding was performed. Liver biopsy with measurement of pressure gradients revealed elevated wedged hepatic vein
pressure, normal free hepatic vein pressure which resulted to a high hepatic venous pressure gradient indicating
portal hypertension.Liver biopsy showed incomplete septal fibrosis (fig 1) and portal vein ectasia (fig 2). Transjugular
intrahepatic portosystemic shunt was placed and the patient did well on diuretics, low salt diet and non selective beta
blockers.
CVID is a rare cause of non cirrhotic portal hypertension (NCPH). Histologic changes can range from hepato-portal
sclerosis , nodular regenerative hyperplasia and incomplete septal cirrhosis. Majority of patients (~90% ) remains
asymptomatic and the mechanism for the development of NCPH remains unclear. Portal vein thrombosis may result
as a secondary event which can often lead to liver decompensation requiring transplantation. Liver biopsy remains the
gold standard in diagnosing NCPH and in identifying typical vascular and architectural changes of NCPH.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Jean Ong Kian Koc : ACG Member
Victor Navarro : ACG Member
Ronald Miick : ACG Non-Member
Incomplete Septal Fibrosis
Portal Vein Ectasia
IMAGE CAPTION: Incomplete Septal Fibrosis Portal Vein Ectasia
(no table selected)
AVERAGE SCORE: 4.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Sita Chokhavatia: [No Comments]|Waqar Qureshi: [No Comments]|Bo Shen: [No Comments]|Marc Zuckerman: [No
Comments]
CONTROL ID: 1746510
TITLE: A case of DRESS syndrome in a middle aged woman
PRESENTER: Saurabh Goyal
PRESENTER (INSTITUTION ONLY): Harlem Hospital Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 51 y/o Hispanic female with history of osteoarthritis and iron deficiency anemia, presented with
progressively worsening epigastric pain, nausea, vomiting, loss of appetite , fatigue and fevers for over two weeks.
She also noticed dark urine and pale colored stools. About a week before, she noticed a rash on her face which
spread to the trunk and extremities sparing palms and soles, prompting her to come to ED. She denied sick contacts
or recent travel history. She also denied toxic habits or herbal medication use. On exam the temperature was 103F.
Cervical lymphadenopathy, epigastric tenderness and generalized erythematous maculopapular non blanching rash
was presenting all over, sparing palms and soles. Labs showed mild leukocytosis with eosinophilia. Liver panel
showed Ast 313, alt 352, Alk P 291, Tbil 2, T bil 1.7. The coagulation profile and platelets were normal. Her measles
IgG Ab was positive. CT abdomen showed no obstruction or mass. On further questioning, patient revealed she was
taking sulfasalazine for one month, which she had borrowed from a friend for arthritis.
A diagnosis of DRESS syndrome was made (Drug reaction, eosinophilia and systemic symptoms).
She was initially started on empiric antibiotics, which were stopped once cultures came back negative and was
managed conservatively. Over the next four days, her enzymes worsened (Ast 1050, Alt 957, Alk P 303) along with
the worsening of the rash. Her serum glucose was normal. Her MELD score was 16 (bilirubin 4.8, INR 1.36,
creatinine 0.3). She was transferred to a tertiary center for evaluation for possible liver transplant. A skin biopsy was
done, which showed interface dermatitis. She was started on steroids with improvement of her clinical picture
including the liver enzymes. She was discharged from the outside facility on tapering dose of steroids.
Discussion: DRESS Syndrome is a rare potentially life threatening, drug induced hypersensitivity reaction causing
rash, eosinophilia, lymphadenopathy and multiple organ involvement (liver, kidneys and lungs). A latency period of
about two to eight weeks is seen between the drug exposure and disease onset. Treatment usually consists of
removing the offending drug and supportive care. It is unclear whether systemic steroids shorten the clinical course
even in patients with acute liver injury. Liver transplant is the only effective therapy for patients with worsening liver
function, not responding to supportive care.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Saurabh Goyal : ACG Non-Member
Frances Charlene Briones : ACG Member
Michael Serlin : ACG Non-Member
Elena Tsai : ACG Member
Joan Culpepper-Morgan : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 5.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Sita Chokhavatia: [No Comments]|Waqar Qureshi: [No Comments]|Bo Shen: [No Comments]|Marc Zuckerman: [No
Comments]
CONTROL ID: 1746511
TITLE: Anabolic-Androgenic Steroid-Induced Cholestasis, Acute Kidney Injury, and Pancreatitis
PRESENTER: Sara Attalla
PRESENTER (INSTITUTION ONLY): Montefiore Medical Center; Albert Einstein College of Medicine
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Anabolic-androgenic steroids (AAS) are a popular class of drugs used to enhance performance and muscle
mass. Its appeal lies in the ability to increase muscle strength through anabolic effects. Cholestasis associated with
AAS is well documented. The alkylated compound increases oral bioavailability and causes impaired biliary secretion,
typically leading to pure cholestasis. Pancreatitis is not a known sequelae of AAS. Renal side effects, although rare,
has been reported in the literature. We report a case of a patient with a history of non-cirrhotic hepatitis C who
presented with jaundice, pancreatitis, and acute kidney injury from AAS. After 3 months of use, he began to
experience abdominal pain, nausea, vomiting, progressive jaundice, and pale stool for 3 weeks. Physical exam was
notable for scleral icterus, epigastric tenderness, and lethargy. Laboratory values demonstrated a BUN of 144 mg/dL,
serum Cr 8 mg/dL, total bilirubin 65.7 mg/dL, AST 50 U/L, ALT 46 U/L, alkaline phosphatase 352 U/L, INR 1.1, and
lipase 2273 U/L. CT abdomen showed prominence of the pancreatic parenchyma with mild stranding and
hepatomegaly without ascites, masses, or ductal dilatation. The patient was medically managed with bicarbonate,
Protonix, N-acetylcysteine infusions and Ursodiol. Liver biopsy was considered but not done given multiple active
medical issues and patient’s bilirubin started to improve with abovementioned care. His pancreatitis was mild and
improved with conservative management. Hemodialysis was done emergently for acidosis and hyperkalemia. At
follow-up one year after hospitalization, his liver tests returned to his baseline with improvement in renal function as
well.
Though cholestatic liver injury has been described in the literature, there is sparse information regarding acute kidney
injury and pancreatitis owing to anabolic-androgenic steroids. Hepatotoxicity with AAS can cause cholestasis and
peliosis hepatis, which is reversible upon discontinuation. Hepatomas have also been reported. What makes this
case unique is its multiorgan involvement. With pancreatitis, no known mechanism of injury has been described, but
ruling out gallstones and eliciting medication and toxin history is important. Focal segmental glomerulosclerosis and
acute tubular necrosis have been described secondary to AAS use. Public awareness and education is needed to
avoid this from occurring. Once exposed to AAS, patients should be followed closely to assess improvement in
clinical parameters and ensure ongoing counseling for abstinence. This rare case demonstrates the atypical and
multiorgan effects of AAS. Early recognition and aggressive supportive care can lead to improved survival.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Sara Attalla : ACG Non-Member
Etan Spira : ACG Non-Member
Mustafa Al Ani : ACG Non-Member
Hatef Massoumi : ACG Non-Member
Harmit Kalia : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Sita Chokhavatia: [No Comments]|Waqar Qureshi: [No Comments]|Bo Shen: [No Comments]|Marc Zuckerman: [No
Comments]
CONTROL ID: 1746595
TITLE: An Uncommon Location of a MRSA Abscess
PRESENTER: Tanima Jana
PRESENTER (INSTITUTION ONLY): University of Texas Health Science Center at Houston
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 31-year-old African-American man presented with 1 week of lower abdominal pain and dysuria. He had
undergone orthotopic liver transplantation 9 years prior for primary sclerosing cholangitis. Other history included
ulcerative colitis and type 2 diabetes. His current immunosuppressive medications included mycophenolate mofetil
(500 mg bid), prednisone (10 mg qday) and tacrolimus (1 mg bid). He had been admitted multiple times in the last
year for partial small bowel obstruction and had recently completed treatment for Clostridium difficile colitis with oral
vancomycin. His vital signs were normal. On physical exam, he was jaundiced and had tenderness to palpation in his
lower abdomen. White cell count was 11,600/mm3, with normal differential. Urinalysis showed 11-20 white blood cells,
positive leukocyte esterase, and negative nitrites. Computed tomography (CT) of the abdomen and pelvis revealed a 3
x 2 cm prostatic abscess. Empiric antibiotic treatment was started with ceftriaxone and vancomycin. No abscess
drainage was performed. Urine culture revealed <10,000 CFU/mL MRSA. Blood cultures grew MRSA in aerobic
bottles. Ceftriaxone was discontinued. He developed acute kidney injury at day 10 and vancomycin was switched to
daptomycin. Transthoracic echocardiogram (TTE) was negative for vegetations. At completion of 6 weeks of
treatment for MRSA, symptoms were resolved, blood and urine cultures were negative, and repeat imaging showed
resolution of the prostatic abscess.
Prostatic abscesses are usually related to gram-negative bacilli and are rarely caused by Staphylococcus Aureus. We
present a unique case of MRSA bacteremia originating from a prostatic abscess. Risk factors for prostatic abscesses
include dialysis, chronic indwelling catheters, immunosuppression, diabetes mellitus, or history of urethral
instrumentation. Our patient’s risk factors included diabetes mellitus and immunosuppression from liver
transplantation. To our knowledge, this is the first case of a prostate abscess in a liver transplant patient. While the
most common post-liver transplant infections involve Cytomegalovirus (CMV), Herpes simplex, Varicella, Candida,
Aspergillus, Cryptococcus, and Histoplasma, our patient was unique in having a MRSA infection. It is debated if
abscess drainage is needed, but our case demonstrates that medical management can be sufficient. Though S.
aureus is a rare cause of genitourinary infections, it should be considered a possible etiologic organism for prostatic
abscess in high-risk patients due to the growing number of invasive MRSA infections in our population.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Tanima Jana : ACG Non-Member
Jorge Machicado : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Sita Chokhavatia: [No Comments]|Waqar Qureshi: [No Comments]|Bo Shen: [No Comments]|Marc Zuckerman: [No
Comments]
CONTROL ID: 1746612
TITLE: Complications in Caroli Disease
PRESENTER: Jennifer Horsley-Silva
PRESENTER (INSTITUTION ONLY): Mayo Clinic Jacksonville Florida
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Caroli disease is a rare inherited disorder characterized by nonobstructive, multifocal areas of saccular
dilatation of intrahepatic biliary ducts. It is thought to be a genetically acquired disease and linked often to autosomal
recessive polycystic kidney disease. It is diagnosed through imaging, and magnetic resonance
cholangiopancreatography (MRCP) is emerging as the diagnostic modality of choice. A 62 year-old female with
previously diagnosed Caroli disease, and Polycystic Kidney Disease presented as a hospital transfer for further
evaluation of a complex liver cyst. Prior to admission she had a complicated course with intermittent severe abdominal
pain that was occurring over the past 3 weeks. Initially when she sought treatment she was provided an oral narcotic
and sent home. The subsequent week she developed fevers and returned to the outside hospital, was admitted,
treated with unknown antibiotics for presumed colitis, and discharged after improvement. A week thereafter, she
developed dyspnea on exertion, ascites, and edema of her lower extremities causing her return to the hospital. During
her second outside hospital admission she was noted to be jaundiced and spiking intermittent fevers. Magnetic
resonance imaging (MRI) was performed which demonstrated a complex liver cyst abutting the upper pole of the right
kidney, which appeared infected. Upon arrival to our facility, blood cultures were obtained, intravenous fluids were
initiated, and Piperacillin-tazobactam was continued. MRI showed a 6.7 cm hepatic cyst in segment VI of the liver with
a fluid level, thickened walls, and edema in surrounding hepatic parenchyma. US guided drainage of 60 ml of purulent
material and fluoroscopic guided 10 french drain was placed via the transhepatic approach. Cyst fluid revealed
aerobic culture showing no growth and anaerobic culture showing Bacteroides fragilis. Patient’s abdominal pain
improved, she remained afebrile and blood cultures were negative. She was subsequently discharged with 6 weeks of
Levofloxacin and Metronidazole with follow up appointments for her hepatic drain to be evaluated and with Infectious
Disease.
Morbidity and mortality from Caroli disease usually comes from complications including cholangitis, hepatolithiasis,
biliary abscesses, sepsis, cirrhosis, portal hypertension, cholangiocarcinoma and renal failure. Prognosis is
determined largely by the frequency and severity of cholangitis, which can cause sepsis or death. This case illustrates
the potential for complications in Caroli disease and the importance of definitive identification of any source of
abdominal pain in these patients. Delay in diagnosis and treatment can lead to significant morbidity and mortality.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Jennifer Horsley-Silva : ACG Non-Member
Katherine Duello : ACG Non-Member
Michael Phillips : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Sita Chokhavatia: [No Comments]|Waqar Qureshi: [No Comments]|Bo Shen: [No Comments]|Marc Zuckerman: [No
Comments]
CONTROL ID: 1746646
TITLE: An Unexpected Cause of Acute Liver Failure
PRESENTER: Brent Lacey
PRESENTER (INSTITUTION ONLY): Naval Medical Center San Diego
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose:
Case
A 66 year-old man with no known liver disease presented with abdominal pain, jaundice, and coagulopathy. He
quickly deteriorated in the ICU, developing distributive shock and DIC. A liver biopsy showed significant hepatocyte
necrosis. During the liver transplant evaluation, a bone marrow biopsy was performed which demonstrated a large
number of hemophagocytic cells, leading to a diagnosis of hemophagocytic lymphohistiocytosis (hemophagocytic
syndrome or HLH). By this point, his condition had continued to worsen and he was deemed to not be a candidate for
either liver transplant or chemotherapy for HLH. In consultation with the family, life support measures were withdrawn.
He expired approximately 24 hours later.
Discussion
HLH is a rare condition that is associated with infections, autoimmune conditions, malignancy, and
lymphoproliferative disorders(1). HLH may mimic more common severe conditions such as septic shock, leukemia,
and severe infections, making it very difficult to diagnose early enough to treat. 85-90% of patients present with fever,
hepatomegaly, and splenomegaly, which may not distinguish them from patients with decompensated cirrhosis(2).
DIC is seen in up to 95% of patients as well.
When the diagnosis of HLH is suspected, a hematology/oncology specialist should be consulted immediately.
Treatment regimens are largely based on pediatric trials, such as the HLH-94 protocol(3), which consists of induction
with dexamethasone and etoposide, along with cyclosporine and/or methotrexate. Even with early recognition, this
condition is highly morbid, with up to 50% mortality(2).
Conclusion
This patient was critically ill very early in his presentation to the liver transplant center. Earlier recognition of this
patient's condition would likely not have made a significant difference in his overall outcome, and he would not have
been a candidate for liver transplant earlier. We acknowledge the difficulty in making this diagnosis and advise that
HLH should be considered in any patient presenting with unexplained liver failure who meets at least 4 out of 9 criteria
for this syndrome.
References
1. Risdall RJ, et al. Virus-associated hemophagocytic syndrome: a benign histiocytic proliferation distinct from
malignant histiocytosis. Cancer. 1979;44(3):993.
2. Henter JI, et al. HLH-2004: Diagnostic and therapeutic guidelines for hemophagocytic lymphohistiocytosis. Pediatr
Blood Cancer 2007;48:124.
3. Henter JI, et al. Treatment of hemophagocytic lymphohistiocytosis with HLH-94 immunochemotherapy and bone
marrow transplantation. Blood. 2002;100(7):2367.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Brent Lacey : ACG Member
Alex Kuo : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Sita Chokhavatia: [No Comments]|Waqar Qureshi: [No Comments]|Bo Shen: [No Comments]|Marc Zuckerman: [No
Comments]
CONTROL ID: 1746682
TITLE: Rectal Variceal Bleeding in a Cirrhotic Patient with Peptic Ulcer Disease
PRESENTER: Sara Attalla
PRESENTER (INSTITUTION ONLY): Montefiore Medical Center; Albert Einstein College of Medicine
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Cirrhosis is a known sequelae of chronic liver disease. Complications include ascites, encephalopathy, and
bleeding varices. Esophageal varices are the most commonly encountered type of bleed, with estimated mortality
from first episode approaching 30-50%. Bleeding ectopic varices can be a rare form of GI bleed in cirrhotics. We
present a case of a 57 year-old man with a history of hepatitis C cirrhosis who presented with melena and coffee
ground emesis. Initial laboratory values were notable for hemoglobin 9.9 g/dL, platelets 158 K/UL, BUN 55 mg/dL,
serum Cr 1.7 mg/dL, total bilirubin 1.8 mg/dL, AST 36 U/L, ALT 27 U/L, and INR 1.4. While in the ER he was noted to
have 4-5 episodes of coffee ground emesis with a drop in hemoglobin by 2 gm. He was transfused packed red blood
cells (PRBCs), started on Protonix and Octreotide drips and underwent emergent esophagogastroduodenoscopy
(EGD). The EGD revealed two small columns of non-bleeding esophageal varices, esophagitis, a clean-based ulcer
in the antrum and an oozing 2-3 cm ulcer with a visible vessel in the second portion of the duodenum, treated with
epinephrine injections and gold-probe cautery. Later that day his mental status deteriorated and he developed
hypotension with a drop in hemoglobin. After endotracheal intubation, initiation of pressor and transfusions support, a
second EGD was performed. The previously bleeding ulcer was again bleeding and was treated with epinephrine
injections and two endo-clips. Over the next hospital day his hemoglobin stabilized between 8-9 g/dL and he was
weaned off pressors. On the fourth day he again became hypotensive and developed hematochezia. A third EGD
revealed the same duodenal ulcer, this time with no stigmata of bleeding. Using the same gastroscope, a flexible
sigmoidoscopy was performed revealing a large rectal varix with a fibrin clot (“nipple sign”). Banding was not
attempted due to the very large nature of the varix. The patient subsequently underwent a transjugular intrahepatic
portosystemic shunt procedure (TIPS). He was stable after TIPS and only required a transfusion of 1 unit of PRBCs
transfusion. Unfortunately, his condition deteriorated in the following days and he succumbed to sepsis and multiorgan failure. There are important points that this case highlights. First, peptic ulcer disease is the most common
etiology of upper GI bleeding. Second, the management of a brisk lower GI bleed, affecting hemodynamics, is EGD
first. Third, TIPS is the appropriate management for bleeding ectopic varices.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Sara Attalla : ACG Non-Member
Akiva Marcus : ACG Member
Mustafa Al Ani : ACG Non-Member
Harmit Kalia : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Sita Chokhavatia: [No Comments]|Waqar Qureshi: [No Comments]|Bo Shen: [No Comments]|Marc Zuckerman: [No
Comments]
CONTROL ID: 1746882
TITLE: A Rare Case of Intrahepatic Extramedullary Hematopoiesis
PRESENTER: Kati Glockenberg
PRESENTER (INSTITUTION ONLY): Department of Medicine New York Presbyterian Hospital - Weill Cornell Medical
Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 54-year-old man with Hepatitis C, transfusion dependent beta-thalassemia, heart failure, pulmonary
hypertension and atrial fibrillation presented with two weeks of epigastric abdominal pain. The pain was cramping in
nature, associated with nausea and abdominal bloating. Home medications included an iron chelator, testosterone,
beta blocker, digoxin, Coumadin and diuretics. On physical exam, the patient was afebrile and hypotensive. He was
jaundiced with hepatomegaly. Labs were notable for elevated AST/ALT, hyperbilirubinemia and elevated AFP of 73.
An abdominal MRI showed hepatic iron deposition and innumerable hepatic lesions similar in signal and enhancement
to known paravertebral extramedullary hematopoietic masses. Given the risk of bleeding, a liver biopsy to rule out
hepatocellular carcinoma was deferred. Hospital course was notable for melena concerning for an upper
gastrointestinal bleed. Endoscopy revealed multiple non-bleeding duodenal ulcers with one bleeding ulcerated mass
in the duodenum that appeared consistent with extramedullary hematopoiesis. The patient subsequently developed
multiorgan system failure secondary to cardiogenic shock and expired.
Beta thalassemia results from decreased or absent production of beta globin chains relative to alpha globin chains in
red blood cells. Alpha chains precipitate within the cell causing ineffective hematopoiesis and chronic hemolysis. This
results in severe anemia clinically manifested by hepatosplenomegaly, bony abnormalities and high output heart
failure (1). Indirect organ damage results from iron overload due to transfusions and stimulation of increased iron
absorption from the gut. Ineffective erythropoiesis leads to compensatory extramedullary erythropoiesis (EM) in which
erythroid colonies form outside of the bone marrow. EM is most common in chronic hemolytic anemias, but can also
occur in myeloproliferative disorders (3). The liver, spleen and lymph nodes are common sites of EM (2). Usually
asymptomatic, EM can cause pain and compression of soft-tissue structures secondary to growth of tumor-like
masses. Treatment options include blood transfusions, surgery, radiotherapy and hydroxyurea. Intrahepatic
extramedullary hematopoietic lesions may be solitary or multiple. Appearance of lesions on MRI varies and may be
influenced by iron deposition and fibrous and fatty components of hematopoietic tissue (4). This case highlights the
importance of considering extramedullary hematopoiesis in the differential diagnosis of intrahepatic lesions in patients
with hemolytic and myeloproliferative disorders, and the importance of understanding and treating the clinical sequela
of such lesions.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Kati Glockenberg : ACG Non-Member
Nikhil Kumta : ACG Member
David Wan : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Sita Chokhavatia: [No Comments]|Waqar Qureshi: [No Comments]|Bo Shen: [No Comments]|Marc Zuckerman: [No
Comments]
CONTROL ID: 1746948
TITLE: Zieve Syndrome: A case report.
PRESENTER: Neha Nigam
PRESENTER (INSTITUTION ONLY): Medstar Georgetown University Hospital
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Zieve Syndrome refers to the constellation of jaundice, hyperlipidemia, and hemolytic anemia in association
with alcoholic fatty liver disease and cirrhosis. Since first described in 1958, very few cases have been reported
despite the large number of cirrhotics admitted after acute alcohol ingestion. We present such a case to avoid
misdiagnosis of Zieve syndrome as persistent obstructive jaundice, and offer a possible explanation for acute lipemia
and hemolysis in liver patients.
A 35-year-old Caucasian male with history of alcoholism, chronic pancreatitis, and cholecystectomy for recurrent
cholelithiasis presented with one week of abdominal pain, jaundice and anorexia. He consumed a pint of vodka daily
during prior weeks. Physical exam revealed diffuse jaundice, spider angiomata, telangiectasias and ecchymoses on
the chest and extremities. Hepatomegaly and tenderness in the right upper quadrant and epigastrium were noted.
Laboratory results showed increased aspartate transaminase (445), alanine transaminase (62), total bilirubin (21.2),
direct bilirubin (16.5) and ethanol level (416). Coagulopathy was noted (INR 6.9). LDH was elevated (351) with low
haptoglobin and increased reticulocyte count (2.5%). Fibrinogen was elevated (458). A peripheral smear showed
occasional spherocytes. Lipid panel showed an increase in total cholesterol (260) and triglycerides (975) from
baseline values. A computed tomography scan revealed hepatomegaly with cirrhotic morphology, fatty infiltration and
no ascites. Magnetic resonance cholangiopancreatography confirmed no biliary dilation. The patient was treated for
alcohol withdrawal and discharged on Pentoxifylline.
Abnormalities in hemoglobin, reticulocyte count, cholesterol and bilirubin are defining factors in Zieve Syndrome with
improvement to near normal values in the third week. The total (33.7) and direct bilirubin (29) increased during the first
week, fitting the ‘regurgitation-type’ jaundice originally described. Triglycerides and total cholesterol quickly decreased
to 598 and 260, respectively. He also had a 2.3 mg/dl drop in hemoglobin, and an elevated LDH with low haptoglobin
suggesting hemolysis. Our differential for the anemia and hemolysis included disseminated intravascular coagulation
(DIC), immunohemolytic anemia and alcoholic hepatitis. However, persistently high fibrinogen ruled out DIC, negative
direct and indirect Coombs tests excluded immunohemolytic anemia, and previous work up for hereditary
spherocytosis was negative. Although treated for alcoholic hepatitis based on an elevated Maddrey's Discriminant
Function, clinical stigmata such as fever, leukocytosis, ascites and encephalopathy were absent suggesting Zieve
Syndrome.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Neha Nigam : ACG Non-Member
Shervin Shafa : ACG Member
James Lewis : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Sita Chokhavatia: [No Comments]|Waqar Qureshi: [No Comments]|Bo Shen: [No Comments]|Marc Zuckerman: [No
Comments]
CONTROL ID: 1746989
TITLE: Severe Cholestatic Drug-induced Liver Injury secondary to Herbal Supplement Artemisinin
PRESENTER: Shiva Kumar
PRESENTER (INSTITUTION ONLY): Aurora St. Luke's Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 43 year old woman presented with a one week history of fatigue, jaundice, dark urine and pruritus.
Physical examination revealed scleral icterus, mild hepatomegaly and no stigmata of chronic liver disease. Past
medical history was umremarkable except for endometriosis and she was on no prescription medications. Laboratory
tests revealed: Br 31.5 (Direct Br 26.2) , ALT 1352, AST 902, ALP 771, INR 1.7. Imaging studies revealed a
heterogenous appearing liver on ultrasonography and MRI abdomen with contrast. MRCP showed a normal appearing
biliary tree. Extensive serologic testing revealed negative markers to hepatotropic and non hepatotropic viruses,
negative autoimmune markers and normal iron indices, ceruloplasmin and alpha1 antitrypsin levels. A liver biopsy was
performed that revealed marked cholestatic hepatitis characterized by a diffuse lobular injury pattern with prominent
cholestasis (Images 1 & 2). There was a mild mixed portal inflammation with intact limiting plates and no significant
fibrosis. The lobules had marked reactive changes with cholestasis, scattered acidophil bodies and inflammation,
including lymphocytes and neutrophils. Upon further questioning, she admitted to taking a herbal supplement
containing Artemisinin for a variety of somatic complaints including headache, starting about 37 days prior to her
presentation.The patient had been taking an equivalent amount of 400 mg of Artemisinin daily.
A diagnosis of severe cholestatic drug induced liver injury was made. Pruritus was treated by cholestyramine and
hydroxyzine. Her subsequent clinical course was characterized by gradual clinical and biochemical improvement
(Table 1). At the time of this case report, 10 weeks after her initial presentation, she remains asymptomatic and her
laboratory tests showed Total Br 9.0, AST 131, ALT 190, ALP 477 and INR 1.0.
Artemisinin is a chinese herbal supplement with activity against many forms of malarial organisms. Artemisinin
derivatives have been rarely associated with idiosyncratic acute liver injury. Although the precise mechanism of liver
injury is unclear, Artemisinin is extensively metabolized by the liver and hepatotoxicty is likely secondary to an
idiosyncratic immunological reaction to a hepatic metabolite. Herbal supplements remain a common and often underrecognized cause of idiosyncratic drug induced acute liver injury. A careful medication and supplement history is
essential in establishing a diagnosis of drug induced liver injury in suspected cases.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Shiva Kumar : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Sita Chokhavatia: [No Comments]|Waqar Qureshi: [No Comments]|Bo Shen: [No Comments]|Marc Zuckerman: [No
Comments]
CONTROL ID: 1746992
TITLE: Non-cirrhotic portal hypertension from chemotherapy-induced intrahepatic non-tumorous arterioportal fistula
PRESENTER: Melissa Martinez Mateo
PRESENTER (INSTITUTION ONLY): Indiana University School of Medicine
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Intrahepatic arterioportal fistulas (APF) are rare, are mostly caused by trauma or malignancy, and can cause
presinusoidal portal hypertension. We report a case of Chemotherapy-induced non-tumoral intrahepatic APF (CI-APF)
presenting with non-cirrhotic portal hypertension (NCPH).
A 57-year-old white man presented with chronic abdominal pain and abnormal liver tests for one year (3/13). He
underwent right hemicolectomy for cecal adenocarcinoma (2/12) and received adjuvant chemotherapy with FOLFOX
(4/12-9/12). His laboratory data showed thrombocytopenia and fluctuating liver tests (AST 43-90 U/L; ALT 49-91U/L;
alkaline phosphatase 173-280U/L and total bilirubin 0.4-1.7mg/dL). Viral and autoimmune hepatitis were excluded.
Physical exam was normal. Upper endoscopy showed new trace esophageal varices. Abdominal magnetic resonance
imaging reported a large APF in both lobes of the liver with hyperarterial vascularity perfusing the right hepatic lobe,
early shunting to the portal vein, moderate atrophy of right lobe of the liver, distension of the portal vein and
splenomegaly with otherwise patent hepatic vasculature (A). Trans-jugular liver biopsy with wedge pressure and
hepatic arteriography showed hepatic vein pressure gradient of 3mmHg and hepatic arterial to portal vein shunting
(B). Liver biopsy notable for focal sinusoidal dilatation, unremarkable bile ducts, portal tracts and hepatocytes with no
fibrosis. Prior imaging showed normal hepatic anatomy (2/2012, 6/2012), and fatty infiltration of the liver without
vascular abnormalities (11/2012). The occurrence of APF with pre-sinusoidal portal hypertension and the temporal
relationship with chemotherapy led to the final diagnosis of NCPH from CI-APF.
Several cases of NCPH in patients undergoing chemotherapy for metastatic colorectal cancer have been reported. It
is believed that severe hepatic injury from chemotherapy results in benign transformation of the hepatic parenchyma
into nodular regenerative hyperplasia (NRH). In our case, the presence of pre-sinusoidal portal hypertension is more
supportive of obliterative portal venopathy leading to APF rather than NRH. Shunt reduction with minimally invasive
techniques such as transcatheter hepatic artery embolization have been successfully performed without severe
complications.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Melissa Martinez Mateo : ACG Non-Member
David Agarwal : ACG Non-Member
Raj Vuppalanchi : ACG Member
IMAGE CAPTION:
(no table selected)
AVERAGE SCORE: 5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Sita Chokhavatia: [No Comments]|Waqar Qureshi: [No Comments]|Bo Shen: [No Comments]|Marc Zuckerman: [No
Comments]
CONTROL ID: 1747028
TITLE: A Case of Drug Induced Liver Injury arising from Ripped Fuel.
PRESENTER: Hye Yeon Jhun
PRESENTER (INSTITUTION ONLY): The Methodist Hospital
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: “Ripped Fuel” is an advanced weight loss and fat burning formula, containing herbal extract with 60%
flavonoids, caffeine, and cacao. Although it has been known to have good safety profile, we present a case that
illustrates drug induced liver injury secondary to its use. A 36-year-old female with history of depression and no prior
liver disease presented with 1-week history of abdominal pain, anorexia, and nausea. She began to take “Ripped
Fuel” 3 weeks prior to developing these symptoms to loose weight. She denied use of other herbal medicine,
supplements, or acetaminophen. For her depression, she had been taking venlafaxine for years with no recent
changes in medications. On physical examination, she had scleral icterus and mild jaundice. Abdominal examination
revealed mild RUQ tenderness with no hepatosplenomegaly and no stigmata of chronic liver disease. Initial laboratory
findings suggested fulminant hepatic failure with AST 2152 U/L, ALT 2711 U/L, ALP 290 U/L, total bilirubin 3.4 mg/dL,
direct bilirubin 2.4 mg/dL, INR 1.2, BUN 10 mg/dL, and creatinine 0.7 mg/dL. Acute hepatitis panel was consistent
with previous immunization to hepatitis A and hepatitis B and was negative for hepatitis C. Autoimmune work up with
anti-smooth muscle antibody, anti-mitochondrial antibody, immunoglobulin G, A, M levels were all within normal limits.
ANA was 1:80. As the liver enzymes continued to escalate with AST of 2511 U/L, and ALT of 2925 U/L, liver biopsy
was performed on hospital day 3. Findings of the liver biopsy was consistent with marked portal inflammation with
circumferential interface activity and bridging hepatocyte necrosis, consistent with drug induced liver injury (DILI). She
was started on methylprednisone 60mg/day and ursodeoxycholic acid (UDCA) 1000mg/day, and her AST, ALT levels
began to improve instantly after beginning treatment. There was a lag of improvement in the level of bilirubin, which
began to trend down 3 days after steroid treatment. She continued to improve clinically, with no evidence of hepatic
failure during hospitalization and was safely discharged. Discussion : Flavonoids have been described to cause
significant liver injury in several case reports. Treatment after development of DILI has been poorly defined, besides
discontinuing the triggering substance. Previously, steroids have been studied to prevent tissue damage from
inflammatory response, which failed to show beneficial effects. Usage of UDCA has been shown to be favorable, due
to protection of hepatocytes against cytotoxic effects of bile acids and stimulating hepatobiliary secretion. Recently,
combination of steroids and UDCA proved to benefit the outcome of patients with severe DILI.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: Yes
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Hye Yeon Jhun : ACG Non-Member
Kongkiat Chaikriangkrai : ACG Non-Member
Wei-Chung Chen : ACG Non-Member
Abimbola Aderinto : ACG Non-Member
Howard Monsour : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Sita Chokhavatia: [No Comments]|Waqar Qureshi: [No Comments]|Bo Shen: [No Comments]|Marc Zuckerman: [No
Comments]
CONTROL ID: 1747089
TITLE: Hypercalcemia in chronic liver disease, A Rare Entity
PRESENTER: Rafia Zulfikar
PRESENTER (INSTITUTION ONLY): Geisinger medical centre
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Chronic liver disease is usually associated with hypocalcemia as a result of hypoalbuminemia. We present a
rare case of chronic liver disease associated with hypercalcemia. Hypercalcemia in chronic liver disease in absence of
hepatoma is an extremely rare and a poorly understood entity with only 17 cases reported in literature
Methods: We present a 50 year old female with hemochromatosis induced liver cirrhosis who was admitted with
abdominal pain following peritoneal tap. She had an expanding anterior wall hematoma confirmed by CT scan. On
examination she was grossly icteric but not encephalopathic. Labs revealed worsening liver enzymes. Total bilirubin
peaked around 10 days at 31.6 before starting to trend down. She also had new onset hypercalcemia (Serum calcium
12) during this admission. Extensive evaluation of hypercalcemia was pursued. Her PTH was appropriately
suppressed and Vitamin D was low ruling out parathyroid adenoma or Vitamin D toxicity. PTH-rP and AFP were
normal as was TSH and T4 ruling out malignancy and hyperthyroidism as etiology. Normal BUN and low to normal
bicarbonate ruled out renal etiology for hypercalcemia. Imaging was negative for granulomatous disease process. No
family history or personal history of colon cancer or familial hypocalciuric hypercalcemia. She had not been bed bound
for long period. After extensive work up for usual causes, hypercalcemia was thought to be secondary to chronic liver
disease worsened by acute illness. Interestingly her hypercalcemia gradually resolved later as her bilirubin improved
confirming our suspicion.
Results: Hypercalcemia induced by advanced chronic liver disease is a poorly understood phenomenon and a
diagnosis of exclusion. It is associated with high bilirubin levels and the serum calcium can reach very high levels.
With elevated total Bilirubin there is direct effect and also indirect effect with down regulation of Osteogenic factors
like RUNX2 and upregulation of Osteoclastogenesis factors like RANKL/OPG gene expression. This causes
increased bone turn over and loss of calcium causing hypercalcemia. Also with development of renal failure or
hepatorenal syndrome patients have decreased renal excretion and may develop hypercalcemia. Calcium level
improves with improvement of bilirubin and is responsive to bisphosphonate treatment
Conclusion: Hypercalcemia induced by advanced chronic liver disease without hepatoma is an exquisitely rare
condition with only 17 cases described to date in the literature. Clinician awareness is essential to pick this rare entity
as early bisphophonate treatment leads to resolution of hypercalcemia and better outcome.
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Rafia Zulfikar : ACG Non-Member
Alok Silodia : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Sita Chokhavatia: [No Comments]|Waqar Qureshi: [No Comments]|Bo Shen: [No Comments]|Marc Zuckerman: [No
Comments]
CONTROL ID: 1747153
TITLE: Use of Telaprevir to Treat Hepatitis C Recurrence after Liver Transplantation in an HIV Co-infected Patient
PRESENTER: Gurshawn Singh
PRESENTER (INSTITUTION ONLY): Cleveland Clinic Foundation
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: A 62-year-old Caucasian male with HIV, and chronic HCV genotype 1b complicated by cirrhosis and
hepatocellular carcinoma, underwent OLT. He developed recurrent hepatitis C 9 months post-transplantation. HAART
regimen included emtricitabine-tenofovir 200-300 mg daily, etravirine 200 mg BID, and darunavir-ritonavir 600 mg-100
mg BID due to previously failed therapy and HIV resistance. CD4 count was 461 cells/μL and he was negative for HIV1 RNA by PCR. His immunosuppression regimen consisted of tacrolimus 0.5 mg every 15 days (while on HIV
protease inhibitors) and mycophenolate mofetil 500 mg bid. His transaminases were in the 150-300 U/L range.
Baseline HCV RNA was at 4,920,000 IU/mL and interleukin 28B genotype was CT. Prior to starting TVR-based triple
therapy, we stopped darunavir-ritonavir and started raltegravir 400 mg BID to avoid having the patient on both HCV
and HIV protease inhibitors. His tacrolimus level was increased to 0.5 mg BID during the transition.
On day 1 of TVR-based therapy, patient was started on TVR 750 mg TID, ribavirin 400 mg BID and pegylated
interferon α2a 180 mcg weekly. In addition, he took 0.5 mg of tacrolimus and the tacrolimus level was checked at 12
and 24 hours and every other day thereafter for 2 weeks. Tacrolimus goal level was 4-6 ng/mL. The mean area under
the concentration time curve (AUC) for tacrolimus while on TVR was 348 ng.hr/mL compared to an expected AUC of
67 ng.hr/mL without TVR. Highest tacrolimus level encountered was 10 ng/mL (12 hours after the initial dose).
Maintenance dose of tacrolimus while on TVR was 0.5 mg every 5 days. HCV RNA was not quantifiable (< 43 IU/mL)
at week 4 of HCV therapy and was undetectable at week 8. He completed 12-weeks of telaprevir, continued on
ribavirin/pegylated interferon α2a, and switched back to his HAART regimen. HCV RNA remained negative at week
24.
This case demonstrates that telaprevir-based triple therapy can be used to treat HCV recurrence in HIV co-infected
patients with frequent adjustments to tacrolimus dosage.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: Yes
Initiated Research: Investigator
Financial Relationships: Yes
Extra Info: : Dr. Alkhouri - Consultant/speaker: Vertex Pharmaceuticals Incorporated
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Gurshawn Singh : ACG Non-Member
William Carey : ACG Member
Nizar Zein : ACG Member
Alan Taege : ACG Non-Member
Naim Alkhouri : ACG Member
Different treatment time points and changes to tacrolimus dose
IMAGE CAPTION: Different treatment time points and changes to tacrolimus dose
Laboratory tests and virological responses
Test
Baseline
Week 4
Week 12
Week 16
HCV RNA
4,920,000
< 43
undetectable
undetectable
undetectable
667
367
undetectable
14.6
13
11.9
12.6
2660
2080
2130
1800
126
107
99
103
0.95
1.12
0.94
0.93
ALT (U/L)
126
48
39
28
AST (U/L)
86
46
28
30
(IU/mL)
HIV RNA
(copies/mL)
hemoglobin
(g/dL)
Absolute
neutrophil count
(uL)
Platelets
(10^3/uL)
Creatinine
(mg/dL)
TABLE TITLE: Laboratory tests and virological responses
AVERAGE SCORE: 4.5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Sita Chokhavatia: [No Comments]|Waqar Qureshi: [No Comments]|Bo Shen: [No Comments]|Marc Zuckerman: [No
Comments]
CONTROL ID: 1747154
TITLE: An Unusual Cystic Mass Of The Liver
PRESENTER: Meghan NeSmith
PRESENTER (INSTITUTION ONLY): Oregon Health and Science University
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Clinical Presentation:
A 43 year old female with a history of migraines and hypertension presented with three months of dull, constant, right
upper quadrant abdominal pain with no associated symptoms. She denied weight loss. Exam was significant for a
nontender abdomen without hepatosplenomegaly and no stigmata of chronic liver disease. Significant labs were: Cr
0.7, Alb 4, AST 17, ALT 14, AP 64, TB 0.24. A RUQ ultrasound showed a hypoechoic mass appearing in the right lobe
of the liver. An abdominal CT revealed a heterogeneous appearing cyst in the liver with no evidence of ascites. An
EGD was performed for evaluation of her abdominal pain, which showed esophagitis. A PPI was started but she
continued to have abdominal pain after several weeks of treatment. An MRI was obtained to further characterize the
hepatic cyst, and revealed a 3.9 x 4.3 x 5.1 cm circumscribed cyst within segment 4b which contained a large
enhancing complex mural nodule of 3.2 cm in diameter. The mural nodule was composed of multiple thin and thick
septations surrounding tiny cystic spaces. Echinococcus antibodies were weakly positive. She was referred for
hepatobiliary surgical consultation. She was given preoperative albendazole for the possibility of an Echinococcal cyst.
A left hepatectomy and cholecystectomy were successfully performed after several days of albendazole. Surgical
findings were significant for a large, mildly steatotic liver with the cyst located predominantly in segment 4b, but also
extending into segment 3. Surgical pathology revealed a 5 cm multilocated mucinous biliary cystadenoma, lined by
simple cuboidal to columnar mucinous epithelium with ovarian-type stroma, which was negative for malignancy.
Immunohistochemical studies showed stromal spindle cells positive for ER and PR.
Discussion:
Biliary cystadenomas are rare, slow-growing hepatic neoplasms that typically occur in middle aged women and
account for less than 5% of cystic lesions of the liver. The clinical symptoms can be nonspecific, but often include
abdominal pain. Cystadenomas have the potential for malignant transformation with progression to biliary
cystadenocarcinomas, which can be focal and undetectable on imaging. Patients with a suspected cystadenoma
should be promptly referred for surgical resection due to the potential for progressing to malignancy and a high risk of
recurrence with non-surgical management strategies.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Meghan NeSmith : ACG Non-Member
Travis Smith : ACG Non-Member
Susan Orloff : ACG Non-Member
Joseph Ahn : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.25
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Sita Chokhavatia: [No Comments]|Waqar Qureshi: [No Comments]|Bo Shen: [No Comments]|Marc Zuckerman: [No
Comments]
CONTROL ID: 1747193
TITLE: Serotonin Syndrome in the Endoscopy Suite: The Clinical Importance of an Accurate Medication Reconciliation
PRESENTER: Ryan Gaffney
PRESENTER (INSTITUTION ONLY): Penn State Milton S. Hershey Medical Center, Division of Gastroenterology &
Hepatology
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Percutaneous liver biopsy is the most specific test available to assess the nature and severity of liver
disease. US-guidance has allowed this technique to be performed routinely in the outpatient setting. Because of its
invasive nature, pain is considered a common complication. To our knowledge, this is the first reported case of
serotonin syndrome induced by fentanyl for treatment of post-procedure pain in a patient who underwent a
percutaneous liver biopsy.
A 59-year-old white female with relapsed chronic Hepatitis C presented for a surveillance percutaneous liver biopsy
prior to initiating protease inhibitor-based anti-viral therapy. The patient’s home medications included trazodone and
duloxetine. Pre-procedure, she was hemodynamically stable without complaint. A percutaneous liver biopsy was
performed under US-guidance. 10 minutes post-procedure, the patient developed intense right-sided chest pain.
Imaging and laboratory testing was unremarkable. She was medicated with 50 ug of I.V. fentanyl which did not
alleviate her pain. An additional 100 ug of fentanyl was given and 5 minutes later the patient became agitated,
diaphoretic, and hypertensive. Serial examination revealed flushing, diaphoresis, and rigidity. 2 mg of I.V. lorazepam
was administered with marked improvement in her vital signs and symptoms. The patient was admitted to the medical
ICU and remained afebrile during her hospital stay with resolution of her agitation and widespread pain. Although no
specific etiology was found, review of her medications suggested a possible interaction between fentanyl and her
antidepressants. Considering the presentation, a diagnosis of serotonin syndrome was made, and fentanyl was added
to her medication allergy list. The patient was discharged with instructions to restart her antidepressants. Her liver
biopsy results eventually showed mild inflammatory activity with fibrosis.
Serotonin syndrome is a rare but potentially life-threatening adverse drug reaction resulting from the therapeutic use
or intentional over-dose of serotonergic medications alone or in combination. In recent years, phenylpiperidine-like
opioids including fentanyl have been associated with serotonin syndrome through weak serotonin reuptake inhibition.
We propose that clinicians need to be aware of the increased risk of serotonin syndrome in the outpatient endoscopic
setting, especially with the wider use of SSRIs and serotonergic medications available in clinical practice. Stringent
attention must be paid to a patient’s list of medications and allergies. If a patient is taking multiple serotonergic
medications, it is wise to avoid or use with caution the phenylpiperidine opioids for post-operative analgesia.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Ryan Gaffney : ACG Non-Member
Ian Schreibman : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 3.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Sita Chokhavatia: [No Comments]|Waqar Qureshi: [No Comments]|Bo Shen: [No Comments]|Marc Zuckerman: [No
Comments]
CONTROL ID: 1747199
TITLE: Combined Alpha-1-Antitrypsin Deficiency and Iron Overload as Etiology for Cirrhosis: “ A Double Hit”
PRESENTER: Abhishek Seth
PRESENTER (INSTITUTION ONLY): Louisiana State University Health Sciences Center in Shreveport, LA
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Combined alpha-1-antitrypsin deficiency (AAT) and hereditary hemochromatosis (HH) as an etiology for
cirrhosis, has rarely been reported in literature. AAT deficiency leads to a glutamic acid-to-lysine substitution, which
causes abnormal folding and failure of secretion of AAT from the endoplasmic reticulum in hepatocytes and,
potentially, hepatic injury. HH causes excessive absorption of iron which in turn results in its deposition in
parenchymal organs including the liver where it causes micronodular cirrhosis.
Methods: 48-year-old white male with history of hypertension, gastroesophageal reflux disease, hypothyroidism,
chronic back pain, and left renal cyst was referred to the GI clinic by his primary care provider for evaluation of “new
onset cirrhosis”. Review of records revealed elevated transaminases without any derangement of synthetic hepatic
function dating back 3 years. A CT scan of the abdomen for evaluation of a left renal cyst revealed a cirrhotic liver,
prompting referral for evaluation by Gastroenterology. The patient’s only complaint was progressive jaundice. Social
history was significant for alcohol use including 12 beer cans per week for 20 years. Physical exam revealed an
obese male with a BMI of 47.2. Cardiovascular, pulmonary, abdominal, and neurological examination was
unremarkable, including no specific stigmata of liver disease. Laboratory revealed AST 94, ALT 57, ALP 148, total
bilirubin 4.1, and albumin 2.1; iron panel revealed iron 215, TIBC 214, ferritin 929, transferrin saturation 100.
Hemogloblin was 12.1 and INR 2.35. Viral hepatitis serology was negative. Genetic testing for hemochromatosis
revealed single mutation in H63D gene with no mutations in C282Y and 565C genes. Liver biopsy revealed diastase
resistant intracytoplasmic globules in PAS-D stained sections consistent with AAT storage disease, as well as
increased iron storage in hepatocytes (2-3+ iron stain).
Results: N/A
Conclusion: Hereditary hemochromatosis (HH) and AAT deficiency are well known etiologies for cirrhosis in the white
population, however, the diagnosis of both conditions together in one patient is rare. Patients with heterozygous
mutation of H63D gene, are considered to be silent carriers of HH. Whether the coexistent AAT deficiency may
potentiate iron overload and, in turn, liver damage is unclear. Studies exploring the possible association between
these conditions have shown inconsistent results. This case demonstrates the importance of a thorough approach of
evaluation seeking the etiology of liver disease, rather than one only/merely targeting the suspected diagnosis.
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Abhishek Seth : ACG Non-Member
Kenneth Manas : ACG Member
Paul Jordan : ACG Member
Moheb Boktor : ACG Member
Jonathan Alexander : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 4.75
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Sita Chokhavatia: [No Comments]|Waqar Qureshi: [No Comments]|Bo Shen: [No Comments]|Marc Zuckerman: [No
Comments]
CONTROL ID: 1747302
TITLE: Primary Hepatic Leiomyosarcoma: a rare diagnosis with an anticipated outcome.
PRESENTER: Omar Mousa
PRESENTER (INSTITUTION ONLY): State University of New York - Upstate Medical University
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Primary Hepatic Sarcomas (PHS) represent <1% of all hepatic malignancies, and are classified according to
their histologic features. Primary Hepatic Leiomyosarcoma (PHL) is one variant which has poorly characterized
prognostic factors and lacks an optimal management protocol due to its rarity.
We present a case of PHS in a 34 year old African American male. He had a 7 month history of intermittent back pain
before presenting with right upper quadrant abdominal pain, worsening dyspnea and bilateral lower extremity swelling.
On exam he was found to have fever, abdominal distension with a palpable mass in the epigastric area and +3 lower
extremity edema. He had anemia (9.9 g/dL) and abnormal liver function tests. Radiologic imaging revealed a 17 cm
complex mass in the right lobe of the liver. A liver biopsy was performed. Immunohistochemistry revealed tumor cells
reactive for smooth muscle actin and desmin, which was consistent with high-grade Leiomyosarcoma. He underwent
right hepatic lobectomy via a thoracoabdominal approach. A 32 x 23 x 13.5 cm hemihepatectomy specimen was
resected with portions of adherent diaphragm, leaving the diaphragmatic margin free of involvement. Patient
subsequently received chemotherapy with Ifosfamide and mesna for residual tumor which was well tolerated. The
patient is doing relatively well 24 months after tumor resection with no recurrence to date.
This rare case of PHL is one of 30 cases reported in the English literature. Prognosis is influenced by the ability to
resect the tumor completely. Liver transplantation (OLT) in such patients was accompanied by early high recurrence
with poor outcomes after 1 year. In our patient, a good outcome was obtained with resection and chemotherapy
despite having advanced disease. International multi registry efforts need to be established to assess the most
effective therapeutic modalities for PHL.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Omar Mousa : ACG Non-Member
Deborah Forst : ACG Non-Member
Chukwuma Egwim : ACG Member
Scott Zela : ACG Member
Victor Ankoma-Sey : ACG Member
Primary Hepatic Leiomyosarcoma - 32 x 23 x 13.5 cm specimen
IMAGE CAPTION: Primary Hepatic Leiomyosarcoma - 32 x 23 x 13.5 cm specimen
(no table selected)
AVERAGE SCORE: 4.5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Sita Chokhavatia: [No Comments]|Waqar Qureshi: [No Comments]|Bo Shen: [No Comments]|Marc Zuckerman: [No
Comments]
CONTROL ID: 1747309
TITLE: Acute Hepatocellular Damage Secondary To Rituximab-induced Hepatitis
PRESENTER: Hineshkumar Upadhyay
PRESENTER (INSTITUTION ONLY): Jamaica Hospital Medical Center
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction:
Rituximab, an anti-CD 20 monoclonal antibody, is now widely used for the treatment of various hematologic and
autoimmune diseases. Several case studies have reported liver failure/toxicity secondary to reactivation of Hepatitis B
or CMV following treatment with Rituximab. However, there have been few reports of acute liver failure caused directly
by the drug itself. We report a case of acute liver failure in a patient being treated with Rituximab for follicular
lymphoma. The patient was managed conservatively with lab normalization within 2 weeks of cessation of Rituximab.
Case presentation:
A 52-year-old, Caucasian, non-alcoholic male presented to the emergency department with loss of appetite, pale
stools, right upper quadrant pain and dark yellow urine for 4 days. He denied any fever, recent travel and illicit drug
use. The patient was diagnosed with stage IV follicular lymphoma 4 weeks prior and was started on Rituximab 1 week
prior. At that time blood work revealed normal liver function tests. He hadn’t received any other medications or
chemotherapeutic agents.
At current presentation the patient was hemodynamically stable with icteric sclera, axillary and cervical
lymphadenopathy, and exhibited a soft abdomen without any tenderness or organomegaly. Laboratory data revealed
elevated liver enzymes with coagulopathy (ALT-2089 U/L, AST-2165 U/L, total bilirubin-10.5 mg/dl, ALP-271 U/L;
PTT-85.5 seconds, PT -28.9 seconds, INR -2.5). Serum ammonia and acetaminophen levels were normal. Urine and
serum toxicology, hepatitis panel and viral panel including that for CMV were negative. The patient was treated
conservatively and rituximab was discontinued. He improved clinically with labs normalizing within 2 weeks.
Discussion
To the best of our knowledge this is the first case report demonstrating Rituximab-mediated drug induced liver injury in
a patient with lymphoma. The exact mechanism for Rituximab causing direct liver toxicity remains unclear. The
diagnosis is usually clinical and based on patients’ history and laboratory findings after excluding other potential
causes of acute liver failure, including acetaminophen overdose, use of anesthetic agents, acute viral hepatitis and
shock liver. Treatment commonly includes cessation of the drug, however, fulminant cases often require a liver
transplant. Physicians should maintain a high index of suspicion for rituximab-induced hepatitis in patients receiving
the medication who present with compatible symptoms.
Methods: N/A
Results: N/A
Conclusion: N/A
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Oral or Poster
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: No
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Hineshkumar Upadhyay : ACG Non-Member
Khalid Sherani : ACG Non-Member
Abhay Vakil : ACG Non-Member
Kelly Cervellione : ACG Non-Member
Avani Patel : ACG Non-Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Sita Chokhavatia: [No Comments]|Waqar Qureshi: [No Comments]|Bo Shen: [No Comments]|Marc Zuckerman: [No
Comments]
CONTROL ID: 1747479
TITLE: Localized Scleroderma and Autoimmune Hepatitis: A Unique Association
PRESENTER: Geeta Kutty
PRESENTER (INSTITUTION ONLY): John. H Stroger Jr hospital of cook county
PRESENTER (COUNTRY ONLY): United States
ABSTRACT BODY:
Purpose: Introduction:
Autoimmune hepatitis (AIH) is a rare association of systemic sclerosis. Even rarer is the association of AIH with
Localized Scleroderma with only 2 reported cases in literature up to date. We hereby report a case of AIH associated
with localized scleroderma.
Case description:
A 39-year-old female with localized scleroderma presented to the hospital with periumbilical pain, non-bloody emesis
and jaundice. Physical exam showed normal vitals with scleral icterus, thickened skin plaques affecting all extremities,
and a normal abdominal exam. Laboratory findings were significant for a Hg of 10.9gm/dL with an MCV of 74.5 and
Platelets of 143 k/dL. LFTs showed a total protein of 7.3 g/dL with an albumin 3.7 of g/dL, total bilirubin of 9.5 mg/dL ,
AST of 1288 U/L, ALT of 775 U/L, ALP of 184 U/L, GGT of 196 U/L, LDH of 760 U/L and an INR of 1.25. Work up of
chronic liver disease including, serologies for hepatitis A, B and C, EBV, CMV, HSV, Ferritin Iron panel were
unremarkable. Further more autoimmune serologies including antibodies to nuclear, mitochondrial, smooth muscle,
liver cytosol, parietal cells, and liver-kidney microsome type 1 were all negative. Imaging of abdomen and pelvis with
US Doppler and CT scan were unremarkable. Liver biopsy obtained showed plasma cell infiltration, rosette formation
and interface hepatitis histology consistent with autoimmune hepatitis. Patient was started on steroids and
azathioprine with complete normalization of LFTs.
Discussion
Localized scleroderma, a rare autoimmune disorder with female predominance, is associated with other autoimmune
conditions. While the pathological mechanisms remain unclear, activation of the cellular and humoral immune
responses may play a part. Association of AIH and scleroderma has been limited to 2 prior case reports. We suggest
that a liver biopsy be considered in patients with localized scleroderma with persistent elevation of liver enzymes in
the setting of negative autoimmune serologies to make a diagnosis of AIH.
Methods: n/a
Results: n/a
Conclusion: n/a
CURRENT CATEGORY: G. Clinical Vignettes/Case Reports
CURRENT SUB-CATEGORY: E. Liver
PRESENTATION TYPE: Poster Only
ACG Research Grant Support: No
Supported by Industry Grant: No
Commercial Products or Services: No
Initiated Research: Investigator
Financial Relationships: Not Applicable
FDA Approval: No
Designed Study: Investigator
Abstract Author: Investigator
AUTH DESIG: ACG Membership Status <font color="red">*</font>:
Geeta Kutty : ACG Non-Member
Andrew Kim : ACG Member
Asad Rafiq : ACG Member
Attar Bashar : ACG Member
(No Image Selected)
(no table selected)
AVERAGE SCORE: 5
REVIEWER FLAGS: (none)
REVIEWER RECOMMENDATION CODE DESCRIPTION: None
REVIEWER COMMENTS:
Sita Chokhavatia: [No Comments]|Waqar Qureshi: [No Comments]|Bo Shen: [No Comments]|Marc Zuckerman: [No
Comments]