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 GTE is a common ingredient in several dietary supplements, some of which have been withdrawn from the market due to safety concerns. An example of this is Exolise® (Arkopharma, France), a weight loss supplement containing GTE that was withdrawn from the market due to 13 cases of liver injury.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 (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: 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) (no table selected) 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) (no table selected) 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 (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: 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 (No Image Selected) (no table selected) 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 (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: 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: (no table selected) 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 (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: 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 (No Image Selected) (no table selected) 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) (no table selected) 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]