Benign Pancreatic disorders
Raika Jamali M.D.
Gastroenterologist and Hepatologist
Sina Hospital
Tehran University of Medical Sciences
Regulation of Pancreatic Secretion
• Gastric acid is the stimulus for the release of
secretin from the duodenum, which stimulates
the secretion of water and electrolytes from
pancreatic ductal cells.
• Release of cholecystokinin (CCK) from the
duodenum and proximal jejunum is largely
triggered by long-chain fatty acids, certain
essential amino acids (tryptophan,
phenylalanine, valine, methionine), and gastric
acid itself. CCK evokes an enzyme-rich secretion
from acinar cells in the pancreas.
• The parasympathetic nervous system (via the vagus
nerve) exerts significant control over pancreatic
• Secretion evoked by secretin and CCK depends on
permissive roles of vagal afferent and efferent
• Also, vagal stimulation effects the release of
vasoactive intestinal peptide (VIP), a secretin agonist.
• Pancreatic exocrine secretion is influenced by
inhibitory neuropeptides:
– pancreastatin,
pancreatic polypeptide, – enkephalin,
– glucagon,
peptide YY,
– galanin.
neuropeptide Y,
calcitonin gene–related peptides,
• Although pancreatic polypeptide and peptide YY may
act primarily on nerves outside the pancreas,
somatostatin acts at multiple sites.
• The mechanism of action of these various factors has
not been fully defined.
• The ductal cells secrete bicarbonate, derived from
plasma (93%) and intracellular metabolism (7%).
• Bicarbonate enters through the sodium bicarbonate
cotransporter with depolarization caused by chloride
efflux through the cystic fibrosis transmembrane
conductance regulator (CFTR).
• Secretin and VIP, both of which increase intracellular
cyclic AMP, act on the ductal cells opening the CFTR
in promoting secretion.
• CCK potentiates the stimulatory effects of
• Acetylcholine also plays an important role in
ductal cell secretion.
• Bicarbonate helps neutralize gastric acid and
creates the appropriate pH for the activity of
pancreatic enzyme.
• All pancreatic enzymes have pH optima in the
alkaline range.
• The acinar cell is concerned with the secretion
of pancreatic enzymes.
• Proteins synthesized by the endoplasmic
reticulum are processed in the Golgi and then
targeted to the appropriate site, whether that
be zymogen granules, lysosomes, or other cell
• The pancreas secretes amylolytic, lipolytic,
and proteolytic enzymes.
• Amylolytic enzymes such as amylase,
hydrolyze starch to oligosaccharides and to
the disaccharide maltose.
• Lipolytic enzymes include:
– lipase,
– phospholipase A2,
– cholesterol esterase.
• Bile salts inhibit lipase in isolation, but colipase, another
constituent of pancreatic secretion, binds to lipase and
prevents this inhibition.
• Bile salts activate phospholipase A and cholesterol esterase.
• Proteolytic enzymes include:
– endopeptidases (trypsin, chymotrypsin), which act on internal peptide
bonds of proteins;
– exopeptidases (carboxypeptidases, aminopeptidases), which act on
the free carboxyl- and amino-terminal ends of peptides, respectively;
– elastase.
• The proteolytic enzymes are secreted as inactive
precursors and packaged as zymogens.
• Enterokinase, an enzyme found in the duodenal
mucosa, cleaves the lysine-isoleucine bond of
trypsinogen to form trypsin.
• Trypsin then activates the other proteolytic
zymogens in a cascade phenomenon.
• The neurologic stimulation is cholinergic by the
vagus nerve.
• The stimulatory neurotransmitters are acetylcholine
and gastrin-releasing peptides.
• These neurotransmitters activate calcium-dependent
second messenger systems, resulting in the release
of zymogen granules.
• VIP is present in intrapancreatic nerves and
potentiates the effect of acetylcholine.
Autodigestion of the pancreas
• Prevented by the packaging of pancreatic proteases
in precursor form and by the synthesis of protease
inhibitor [i.e., pancreatic secretory trypsin inhibitor (PSTI) or
SPINK1], which can bind and inactivate about 20% of trypsin
• These protease inhibitors are found in:
– the acinar cell,
– the pancreatic secretions,
– the α 1 and α 2 globulin fractions of plasma.
• Loss of any of these protective mechanisms leads to
zymogen activation, autodigestion, and acute
Enteropancreatic Axis and Feedback Inhibition
• Pancreatic enzyme secretion is controlled, by a
negative feedback mechanism induced by
active serine proteases in the duodenum.
• To illustrate, perfusion of the duodenal lumen
with phenylalanine causes a prompt result in
increased plasma CCK levels as well as
increased secretion of pancreatic enzymes.
Acute pancreatitis
• varies from interstitial pancreatitis, which is
usually a mild and self-limited disorder, to
necrotizing pancreatitis, in which the extent
of pancreatic necrosis may correlate with the
severity of the attack and its systemic
Interstitial pancreatitis
Necrotizing pancreatitis
• Common Causes
Gallstones (including microlithiasis)
Alcohol (acute and chronic alcoholism)
Endoscopic retrograde cholangiopancreatography (ERCP),
especially after biliary manometry
Trauma (especially blunt abdominal trauma)
Postoperative (abdominal and nonabdominal operations)
Drugs (azathioprine, 6-mercaptopurine, sulfonamides,
estrogens, tetracycline, valproic acid, anti-HIV medications)
Sphincter of Oddi dysfunction
• Uncommon Causes
– Vascular causes and vasculitis (ischemic-hypoperfusion states after
cardiac surgery)
– Connective tissue disorders
– Thrombotic thrombocytopenic purpura (TTP)
– Cancer of the pancreas
– Hypercalcemia
– Periampullary diverticulum
– Pancreas divisum
– Hereditary pancreatitis
– Cystic fibrosis
– Renal failure
• Rare Causes
– Infections (mumps, coxsackievirus, cytomegalovirus, echovirus, parasites)
– Autoimmune (e.g., Sjögren's syndrome)
• Causes to Consider in Patients with Recurrent Bouts of Acute Pancreatitis
without an Obvious Etiology
– Occult disease of the biliary tree or pancreatic ducts, especially microlithiasis,
– Drugs
– Hypertriglyceridemia
– Pancreas divisum
– Pancreatic cancer
– Sphincter of Oddi dysfunction
– Cystic fibrosis
– Idiopathic
• Autodigestion is a currently accepted pathogenic
• Pancreatitis results when proteolytic enzymes are
activated in the pancreas rather than in the
intestinal lumen.
• A number of factors (e.g., endotoxins, exotoxins,
viral infections, ischemia, anoxia, lysosomal calcium,
and direct trauma) are believed to facilitate
activation of trypsin.
• Activated proteolytic enzymes, especially trypsin,
not only digest pancreatic and peripancreatic
tissues but also can activate other enzymes,(such as
elastase and phospholipase A2).
Activation of Pancreatic Enzymes
• The initial phase is characterized by
intrapancreatic digestive enzyme activation
and acinar cell injury.
• Trypsin activation appears to be mediated by
lysosomal hydrolases such as cathepsin B that
become colocalized with digestive enzymes in
intracellular organelles;
• it is currently believed that acinar cell injury is
the consequence of trypsin activation.
• The second phase of pancreatitis involves the
activation, chemoattraction, and
sequestration of leukocytes and macrophages
in the pancreas, resulting in an enhanced
intrapancreatic inflammatory reaction.
• The third phase of pancreatitis is due to the
effects of cytokines, released by the inflamed
pancreas, on distant organs.
Systemic circulation
PSTI + Trypsin
Alfa2 + Trypsin
Alfa1-AT + Trypsin
Enzyme Y
Prophospholipase A2
Bone marrow
XII Factor
Phospholipase A2
XIIa Factor
• Activated proteolytic enzymes, especially trypsin,
activate other enzymes such as elastase and
phospholipase A2.
• The active enzymes and cytokines then digest
cellular membranes and cause:
interstitial hemorrhage,
vascular damage,
coagulation necrosis,
fat necrosis,
and parenchymal cell necrosis.
• Cellular injury and death result in the
liberation of bradykinin, vasoactive
substances, and histamine that can produce
vasodilation, increased vascular permeability,
and edema with profound effects on many
• The systemic inflammatory response
syndrome (SIRS) and acute respiratory distress
syndrome (ARDS) as well as multiorgan failure
may occur as a result of this cascade of local
as well as distant effects.
Acute Pancreatitis
• Vascular leakage
• Hypovolemia
• Shock
• Acute renal tubular necrosis
Other leucocyte
Oxygen radicals
• There appear to be a number of genetic factors that
can increase the susceptibility and/or modify the
severity of pancreatic injury in acute pancreatitis.
• Four susceptibility genes have been identified:
– (1) cationic trypsinogen mutations (PRSS1m, R122Hm, and
– (2) pancreatic secretory trypsin inhibitor (SPINK1),
– (3) CFTR,
– (4) monocyte chemotactic protein (MCP-1).
• Experimental and clinical data indicate that MCP-1 may be an
important inflammatory mediator in the early pathologic
process of acute pancreatitis, a determinant of the severity
of the inflammatory response, and a promoter of organ
Approach to the Patient
• Abdominal pain, vary from a mild and
tolerable discomfort and more commonly to
severe, constant, and incapacitating distress.
is steady and boring.
• Is located in the epigastrium and periumbilical
region and often radiates to the back as well
as to the chest, flanks, and lower abdomen.
• More intense when the patient is supine, and
patients may obtain some relief by sitting with
the trunk flexed and knees drawn up.
• Nausea, vomiting, and abdominal distention
due to gastric and intestinal hypomotility and
chemical peritonitis are also frequent
Physical examination
A distressed and anxious patient.
Low-grade fever,
– (1) hypovolemia secondary to exudation of blood and plasma proteins
into the retroperitoneal space and a "retroperitoneal burn" due to
activated proteolytic enzymes;
– (2) increased formation and release of kinin peptides, which cause
vasodilation and increased vascular permeability; and
– (3) systemic effects of proteolytic and lipolytic enzymes released into
the circulation.
• Jaundice occurs infrequently; when present, it
usually is due to edema of the head of the
pancreas with compression of the
intrapancreatic portion of the common bile
• Erythematous skin nodules due to
subcutaneous fat necrosis may occur.
• There are pulmonary findings(In 10–20% of
patients), including:
– Basilar rales,
– Atelectasis,
– Pleural effusion, (frequently left sided)
• Abdominal tenderness and muscle rigidity
• Diminished bowel sounds
• An enlarged pancreas with walled off necrosis
or a pseudocyst may be palpable in the upper
abdomen later in the disease course
• A faint blue discoloration around the
umbilicus (Cullen's sign) may occur as the
result of hemoperitoneum,
• Blue-red-purple or green-brown discoloration
of the flanks (Turner's sign) reflects tissue
catabolism of hemoglobin.
• Grey Turner sign
• Cullen’s sign
Laboratory Data
• Increased level of serum amylase and lipase.
Values threefold or more above normal
virtually clinch the diagnosis if gut perforation,
ischemia, and infarction are excluded.
• No correlation between the severity of
pancreatitis and the degree of lipase and
amylase elevations.
• After three to seven days, total serum amylase
values tend to return toward normal.
• Pancreatic isoamylase and lipase levels may
remain elevated for 7 to 14 days
Markers of Severity within 24 Hours
• SIRS [temperature >38° or < 36°C, Pulse > 90, Tachypnea > 24,
WBC > 12,000]
• Hemoconcentration (Hct >44%)
• BISAP (bedside index of severity in acute pancreatitis)
(B) Blood urea nitrogen (BUN) >22 mg%
(I) Impaired mental status
(S) SIRS: 2/4 present
(A) Age >60 years
(P) Pleural effusion
• Organ Failure
Cardiovascular: systolic BP <90 mmHg, heartrate >130
Pulmonary: Pao2 <60 mmHg
Renal: serum creatinine >2.0 mg%
Gastrointestinal: bleeding >500 mL/24 hours
• Risk Factors
– Age > 60 years
– Obesity, BMI > 30
– Comorbid disease
• Markers during Hospitalization
– Persistent organ failure
– Pancreatic necrosis
– Hospital-acquired infection
Laboratory Data
• Leukocytosis (15,000–20,000 leukocytes per L)
• Hemoconcentration
– with hematocrit values >44%
– and/or blood urea nitrogen (BUN) level >22 mg/Dl
• Hyperglycemia
– decreased insulin release,
– increased glucagon release,
– increased output of adrenal glucocorticoids and
• Hypocalcemia
Laboratory Data
• Hyperbilirubinemia (>4.0 mg/dL) in 10%
– is transient
– return to normal in four to seven days.
• Serum alkaline phosphatase
• and aspartate aminotransferase levels are
also transiently elevated
• Elevated serum lactic dehydrogenase levels
(>500 U/dL)
• Hypertriglyceridemia occurs in 5–10%
• Hypoxemia (arterial Po2 60 mmHg), which
may herald the onset of ARDS.
• Electrocardiogram is occasionally abnormal in
acute pancreatitis with ST-segment and Twave abnormalities simulating myocardial
CT Findings and Grading of Acute Pancreatitis
[CT Severity Index (Ctsi)]
Grade Findings
Normal pancreas: normal size, sharply defined, smooth
contour, homogeneous enhancement, retroperitoneal
peripancreatic fat without enhancement
Focal or diffuse enlargement of the pancreas, contour
may show irregularity, enhancement may be
inhomogeneous but there is no peripancreatic
Peripancreatic inflammation with intrinsic pancreatic
Intrapancreatic or extrapancreatic fluid collections
Two or more large collections or gas in the pancreas or
Necrosis score based on contrast-enhanced CT
Necrosis (%)
CT severity index equals unenhanced CT score
plus necrosis score; 6 = severe disease.
CT Scan of acute pancreatitis
• CT shows
of the
Gall stone pancreatitis by ERCP
• Requires two of the following:
– typical abdominal pain,
– threefold or greater elevation in serum amylase
and/or lipase level,
– and/or confirmatory findings on cross-sectional
abdominal imaging.
Differential diagnosis
(1) perforated viscus, especially peptic ulcer
(2) acute cholecystitis and biliary colic
(3) acute intestinal obstruction
(4) mesenteric vascular occlusion
(5) renal colic
(6) myocardial infarction
(7) dissecting aortic aneurysm
(8) connective tissue disorders with vasculitis
(9) pneumonia
(10) diabetic ketoacidosis.
Local complications
• Necrosis
– Sterile
– Infected
– Walled-off necrosis
• Pancreatic fluid collections
– Pancreatic abscess
– Pancreatic pseudocyst
Local complications
• Obstruction of gastrointestinal tract
(stomach, duodenum, colon)
• Pancreatic ascites
– Disruption of main pancreatic duct
– Leaking pseudocyst
• Involvement of contiguous organs by
necrotizing pancreatitis
– Massive intraperitoneal hemorrhage
– Thrombosis of blood vessels (splenic vein, portal vein)
– Bowel infarction
• Obstructive jaundice
Systemic complications
• Pulmonary
Pleural effusion
Mediastinal abscess
Acute respiratory distress syndrome
• Cardiovascular
Sudden death
Nonspecific ST-T changes in electrocardiogram simulating myocardial
• Pericardial effusion
Systemic complications
• Hematologic
– Disseminated intravascular coagulation
• Gastrointestinal hemorrhage
Peptic ulcer disease
Erosive gastritis
Hemorrhagic pancreatic necrosis with erosion into major blood vessels
Portal vein thrombosis, variceal hemorrhage
• Renal
Renal artery and/or renal vein thrombosis
Acute tubular necrosis
Systemic complications
• Metabolic
– Hyperglycemia
– Hypertriglyceridemia
– Hypocalcemia
• Encephalopathy
– Sudden blindness (Purtscher's retinopathy)
– Central nervous system
– Psychosis
• Fat emboli
Fat necrosis
Subcutaneous tissues (erythematous nodules)
Miscellaneous (mediastinum, pleura, nervous system)
Mild Acute Pancreatitis
• The majority of patients
• No organ failure or only transient organ failure
• Will respond to simple supportive care :
– bowel rest,
– intravenous hydration with crystalloid
– analgesia.
• Oral intake can be resumed once the patient
essentially pain free
has no nausea or vomiting,
normal bowel sounds,
and is hungry.
• Typically, a clear liquid diet has been
recommended for the initial meal,
• but a low-fat solid diet is a reasonable choice
following recovery
• Patients with gallstone pancreatitis are at
increased risk of recurrence.
• Therefore, laparoscopic cholecystectomy
during the same admission is recommended.
• An alternative for patients who are not
surgical candidates would be to perform an
endoscopic biliary sphincterotomy.
Severe Acute Pancreatitis
• Vigorous fluid resuscitation take place.
• Measurement of hematocrit and BUN every
12 hours is recommended to ensure adequacy
of fluid resuscitation.
• A decrease in hematocrit and BUN during the
first 12 to 24 hours is strong evidence that
sufficient fluids are being administered
• Patients with persistent organ failure that
does not respond to increased fluids and/or
nasal oxygen to overcome hypoxemia as well
as those patients with labored respirations
that may herald respiratory failure should be
transferred to an intensive care unit for
aggressive hydration and close monitoring for
the possible need of intubation with
mechanical ventilation, hemodialysis, and
support of blood pressure.
Chronic Pancreatitis
Pancreatic Exocrine Insufficiency
• Irreversible damage to the pancreas as
distinct from the reversible changes noted in
acute pancreatitis.
• The presence of histologic abnormalities:
– chronic inflammation,
– fibrosis,
– progressive destruction of both exocrine and
eventually endocrine tissue
Tigar-O Classification System
• Toxic-metabolic
Tobacco smoking
Chronic renal failure
Medications—phenacetin abuse
Toxins—organotin compounds (e.g., DBTC)
• Idiopathic
– Early onset
– Late onset
– Tropical
Tigar-O Classification System
• Genetic
Hereditary pancreatitis
Cationic trypsinogen
CFTR mutations
SPINK1 mutations
• Autoimmune
Isolated autoimmune chronic pancreatitis
Autoimmune chronic pancreatitis associated with Sjögren's syndrome
Inflammatory bowel disease
Primary biliary cirrhosis
Tigar-O Classification System
• Recurrent and Severe Acute Pancreatitis
Postnecrotic (severe acute pancreatitis)
Recurrent acute pancreatitis
Vascular diseases/ischemia
• Obstructive
Pancreas divisum
Sphincter of Oddi disorders (controversial)
Duct obstruction (e.g., tumor)
Preampullary duodenal wall cysts
Posttraumatic pancreatic duct scars
• Alcohol has a direct toxic effect on the
• While patients with alcohol-induced
pancreatitis generally consume large amounts
of alcohol, some consume as little as 50 g/d.
• Prolonged consumption of socially
acceptable amounts of alcohol is compatible
with the development of chronic pancreatitis.
• Cigarette smoke leads to an increased
susceptibility to pancreatic self-digestion and
predisposes to dysregulation of duct cell CFTR
• It has become increasingly apparent that
smoking is an independent, dose-dependent
risk factor.
• Pancreatic stellate cells (PSC) are believed to
play a role in maintaining normal pancreatic
architecture that can shift toward fibrogenesis
in the case of chronic pancreatitis
• Alcohol or additional stimuli lead to matrix
metalloproteinase–mediated destruction of
normal collagen in pancreatic parenchyma,
which later allows for pancreatic remodeling.
• Proinflammatory cytokines (TNFα, ILB-1, IL-6)
as well as oxidant complexes are able to
induce PSC activity with subsequent new
collagen synthesis.
• PSCs also possess transforming growth factor
B–mediated self-activating autocrine
pathways that may explain disease
progression in chronic pancreatitis even after
removal of noxious stimuli.
Etiologic Considerations
• Alcoholism is the most common cause of
clinically apparent chronic pancreatitis,
• While cystic fibrosis is the most frequent
cause in children
• Idiopathic chronic pancreatitis.
– up to 15% of patients with idiopathic pancreatitis
may have pancreatitis due to genetic defects
Hereditary chronic pancreatitis
• Gene encoding for trypsinogen.
• The defect prevents the destruction of
trypsinogen and allows it to be resistant to the
effect of trypsin inhibitor, become
spontaneously activated, and to remain
• Mutations of CFTR.
• This gene functions as a cyclic AMP–regulated
chloride channel.
• In patients with cystic fibrosis, the high
concentration of macromolecules can block
the pancreatic ducts
• 1000 putative mutations of the CFTR gene
Monosymptomatic form of cystic fibrosis
(chronic pancreatitis)
• Patients were adults when the diagnosis of
pancreatitis was made;
• None had any clinical evidence of pulmonary
• Sweat test results were not diagnostic of
cystic fibrosis.
• Combination of two CFTR mutations and an
N34S SPINK1 mutation increased the risk of
pancreatitis 900-fold
Autoimmune Pancreatitis
• Mild symptoms usually abdominal pain, but without frequent
attacks of pancreatitis,
• Presentation with obstructive jaundice
• Diffuse swelling and enlargement of the pancreas, especially
the head, the latter mimicking carcinoma of the pancreas
• Diffuse irregular narrowing of the pancreatic duct in ERCP
• Increased levels of serum gamma globulins especially IgG4
• Presence of other autoantibodies (ANA,RF)
• Can occur with other autoimmune diseases: Sjögren's
syndrome, primary sclerosing cholangitis, ulcerative colitis,
rheumatoid arthritis
Autoimmune Pancreatitis
• Extra pancreatic bile duct changes such as stricture of the
common bile duct and intrahepatic ducts
• Absence of pancreatic calcifications or cysts
• Pancreatic biopsies reveal extensive fibrosis and
lymphoplasmacytic infiltration
• Glucocorticoids are effective in alleviating symptoms,
decreasing size of the pancreas, and reversing histopathologic
• Two-thirds of patients present with either obstructive
jaundice or a "mass" in the head of the pancreas mimicking
• AIP can be diagnosed with at least one of
three abnormalities:
– (1) diagnostic histology;
– (2) characteristic findings on CT and
pancreatography combined with elevated IgG4
– (3) response to glucocorticoid therapy
Clinical Features
• The abdominal pain may be quite variable in
location, severity, and frequency.
• The pain can be constant or intermittent with
frequent pain-free intervals.
• Eating may exacerbate the pain, leading to a
fear of eating with consequent weight loss.
• The spectrum of abdominal pain ranges from
mild to quite severe, with narcotic
dependence as a frequent consequence
Clinical Features
• Maldigestion is manifested as chronic
diarrhea, steatorrhea, weight loss, and
• Patients with chronic abdominal pain may or
may not progress to maldigestion, and 20% of
patients will present with symptoms of
maldigestion without a history of abdominal
• Despite the steatorrhea, clinically apparent
deficiencies of fat-soluble vitamins are
surprisingly uncommon.
Laboratory data
• In contrast to acute pancreatitis, the serum
amylase and lipase levels are usually not
strikingly elevated in chronic pancreatitis.
• Elevation of serum bilirubin and alkaline
phosphatase may indicate cholestasis
secondary to common bile duct stricture
caused by chronic inflammation.
• Many patients have impaired glucose
tolerance with elevated fasting blood glucose
Laboratory data
• Diagnostic test with the best sensitivity and
specificity is the secretin stimulation test.
• It becomes abnormal when 60% of the
pancreatic exocrine function has been lost.
• This usually correlates well with the onset of
chronic abdominal pain.
Laboratory data
• Vitamin B12 malabsorption in 40%. This can
be corrected by the administration of oral
pancreatic enzymes.
• A decrease of fecal elastase level to <100 g
per gram of stool strongly suggests severe
pancreatic exocrine insufficiency.
Imaging studies
• Diffuse calcifications noted on plain film of
the abdomen usually indicate significant
• CT may show calcification, dilated ducts, or an
atrophic pancreas, pseudocyst and pancreatic
• MRCP provides a direct view of the pancreatic
duct and is now the diagnostic procedure of
What are arrows?
CT - chronic pancreatitis
• Whether EUS alone can detect early, noncalcific
chronic pancreatitis with the same degree of
accuracy as the hormone-stimulation test is
• Data comparing these modalities head-to-head have
indicated that EUS is not a sensitive enough test for
detecting early chronic pancreatitis.
• However, recent data suggest that EUS can be
combined with endoscopic pancreatic function
testing (EUS-ePFT) during a single endoscopy to
screen for chronic pancreatitis in patients with
chronic abdominal pain.
Narcotic addiction
Impaired glucose tolerance
Cobalamin malabsorption
Nondiabetic retinopathy
Effusions with high amylase content
Gastrointestinal bleeding
Cholangitis and/or biliary cirrhosis
Subcutaneous fat necrosis
Bone pain
Pancreatic cancer
Annular Pancreas
• When the ventral pancreatic anlage fails to migrate
correctly to make contact with the dorsal anlage,
the result may be a ring of pancreatic tissue
encircling the duodenum.
• Such an annular pancreas may cause intestinal
obstruction in the neonate or the adult.
• Symptoms of postprandial fullness, epigastric pain,
nausea, and vomiting may be present for years
before the diagnosis is entertained.
• The radiographic findings are symmetric dilation of
the proximal duodenum with bulging of the recesses
on either side of the annular band, effacement but
not destruction of the duodenal mucosa,
accentuation of the findings in the right anterior
oblique position, and lack of change on repeated
• The differential diagnosis should include duodenal
webs, tumors of the pancreas or duodenum,
postbulbar peptic ulcer, regional enteritis, and
• Patients with annular pancreas have an increased
incidence of pancreatitis and peptic ulcer.
Pancreas divisum
• Occurs when the embryologic ventral and dorsal
pancreatic anlagen fail to fuse, so that pancreatic
drainage is accomplished mainly through the
accessory papilla.
• Is the most common congenital anatomic variant of
the human pancreas.
• Does not predispose to the development of
pancreatitis in the great majority of patients .
• However, the combination of pancreas divisum and a
small accessory orifice could result in dorsal duct
MRCP of pancreas divisum
• Amylase circulates in the blood in a polymer
form too large to be easily excreted by the
• Elevated serum amylase value, a low urinary
amylase value, and a Cam/Ccr ratio of <1%.
• The presence of macroamylase can be
documented by chromatography of the serum
• Documented in a few patients with cirrhosis
or non-Hodgkin's lymphoma.
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