Etiology of acute pancreatitis

Author: Santhi Swaroop Vege, MD

Section Editor: David C Whitcomb, MD, PhD
Deputy Editor: Shilpa Grover, MD, MPH, AGAF

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is
complete.

Literature review current through: Dec 2019. | This topic last updated: Jan 09, 2019.

INTRODUCTION

Acute pancreatitis is an inflammatory condition of the pancreas characterized by

abdominal pain and elevated levels of pancreatic enzymes in the blood. Acute
pancreatitis is a leading gastrointestinal cause of hospitalization in the United
States [1]. Several conditions are associated with acute pancreatitis. Of these
gallstones and chronic alcohol abuse accounting for approximately two-thirds of
cases.

This topic will review the etiology of acute pancreatitis and an approach to
establishing the underlying etiology. Our approach is largely consistent with
guidelines issued by the American Gastroenterological Association and American
College of Gastroenterology and is outlined below. The pathogenesis, clinical
manifestations, diagnosis, and management of acute pancreatitis are discussed
separately. (See "Predicting the severity of acute pancreatitis" and "Management
of acute pancreatitis" and "Pancreatic debridement" and "Pathogenesis of acute
pancreatitis".)

EPIDEMIOLOGY
The reported annual incidence of acute pancreatitis in the United States ranges
from 4.9 to 35 per 100,000 population [2]. The incidence of acute pancreatitis is
increasing worldwide due to increased rates of obesity and gallstones [3].
Smoking may increase the risk for non-gallstone-related pancreatitis by
mechanisms that are unclear and may potentiate alcohol-induced damage to the
pancreas [4-9].

Mortality in acute pancreatitis is usually due to systemic inflammatory response

syndrome and organ failure in the first two-week period, while after two weeks it is
usually due to sepsis and its complications [10,11]. In a systematic review of
studies of acute pancreatitis, overall mortality was approximately 5 percent, with
mortality rates in patients with interstitial, and necrotizing pancreatitis, of 3
percent, and 17 percent, respectively [12]. However, mortality rates in necrotizing
pancreatitis may be lower in centers of expertise (range 6 to 9 percent) [10,13].

ETIOLOGY

Gallstones — Gallstones (including microlithiasis) are the most common cause of

acute pancreatitis accounting for 40 to 70 percent of cases [14]. However, only 3
to 7 percent of patients with gallstones develop pancreatitis [15,16]. The
mechanism by which the passage of gallstones induces pancreatitis is unknown.
Two factors have been suggested as the possible initiating event in gallstone
pancreatitis: reflux of bile into the pancreatic duct due to transient obstruction of
the ampulla during passage of gallstones; or obstruction at the ampulla secondary
to stone(s) or edema resulting from the passage of a stone [17,18].
Cholecystectomy and clearing the common bile duct of stones prevents
recurrence, confirming the cause-and-effect relationship [15].

The risk of developing acute pancreatitis in patients with gallstones is greater in

men; however, the incidence of gallstone pancreatitis is higher in women due to a
higher prevalence of gallstones [15]. Small gallstones are associated with an
increased risk of pancreatitis [19]. One study found that stones with a diameter of
less than 5 mm were significantly more likely than larger stones to pass through
the cystic duct and cause obstruction at the ampulla (see 'Biliary sludge and
microlithiasis' below).

Alcohol — Alcohol is responsible for approximately 25 to 35 percent of cases of

acute pancreatitis in the United States [20]. Approximately 10 percent of chronic
alcoholics develop attacks of clinically acute pancreatitis that are
indistinguishable from other forms of acute pancreatitis.

Alcohol may act by increasing the synthesis of enzymes by pancreatic acinar cells
to synthesize the digestive and lysosomal enzymes that are thought to be
responsible for acute pancreatitis or over-sensitization of acini to cholecystokinin
[21,22]. However, the exact mechanism of pancreatic injury, the genetic and
environmental factors that influence the development of pancreatitis in alcoholics,
and the reason why only a small proportion of alcoholics develop pancreatitis, are
unclear. (See "Pathogenesis of acute pancreatitis".)

There is debate about the presence of underlying chronic pancreatitis in patients

presenting with acute alcoholic pancreatitis. It was initially thought that alcohol
causes chronic pancreatitis, and that alcoholics who present with clinically acute
pancreatitis have underlying chronic disease [23]. However, long-term follow-up
studies of patients with acute alcoholic pancreatitis have demonstrated that not
all patients progress to chronic pancreatitis, even with continued alcohol abuse
[24]. This suggests that some alcoholics may have nonprogressive acute alcohol-
induced pancreatitis [25].

Hypertriglyceridemia — Serum triglyceride concentrations above 1000 mg/dL (11

mmol/L) can precipitate attacks of acute pancreatitis, although lower levels may
also contribute to severity [26,27]. Hypertriglyceridemia may account for 1 to 14
percent of cases of acute pancreatitis [28,29]. Both primary (genetic) and
secondary (acquired) disorders of lipoprotein metabolism are associated with
hypertriglyceridemia-induced pancreatitis. Acquired causes of
hypertriglyceridemia include obesity, diabetes mellitus, hypothyroidism, pregnancy,
and medications (eg, estrogen or tamoxifen therapy, beta blockers). (See
"Hypertriglyceridemia-induced acute pancreatitis".)

Post-endoscopic retrograde cholangiopancreatography (ERCP) — Acute

pancreatitis occurs in about 3 percent of patients undergoing diagnostic ERCP, 5
percent undergoing therapeutic ERCP, and up to 25 percent undergoing sphincter
of Oddi manometric studies [30]. Multiple operator, patient, and procedure-related
factors increase the risk of post-ERCP pancreatitis. Important risk factors include
lack of ERCP experience, sphincter of Oddi dysfunction, difficult cannulation, and
the performance of a therapeutic (rather than diagnostic) ERCP. (See "Post-
endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis", section on
'Risk factors'.)

Genetic risk — Patients with genetic risk for pancreatitis may present as recurrent
acute pancreatitis, or childhood pancreatitis without a known cause and eventually
progress to chronic pancreatitis. Gain-of-function mutations in the PRSS1 gene,
which encodes cationic trypsinogen, results in an autosomal dominantly inherited
form of hereditary pancreatitis. Mutations in the CFTR gene have been associated
with an autosomal recessively inherited pancreatitis. Pancreatitis has also been
associated with low penetrance mutations in the SPINK1, which may act as a
disease modifier and lower the threshold for developing pancreatitis from other
genetic or environmental factors. Mutations in CTRC gene can cause pancreatitis
with or without associated manifestations of cystic fibrosis [31]. The majority of
"idiopathic" cases appear to have genetic risk, especially in younger patients (age
<35 years). Other genes associated with recurrent acute pancreatitis are
discussed in detail separately. (See "Hereditary pancreatitis", section on
'Genetics'.)
Medications — Pancreatitis due to medications is rare (<5 percent) [32-35]. The
prognosis of drug-induced pancreatitis is generally excellent and mortality is low
[36].

Mechanisms of drug-induced pancreatitis include immunologic reactions (eg, 6-

mercaptopurine, aminosalicylates, sulfonamides), direct toxic effect (eg, diuretics,
sulfonamides), accumulation of a toxic metabolite (eg, valproic acid, didanosine,
pentamidine, tetracycline), ischemia (diuretics, azathioprine), intravascular
thrombosis (eg, estrogen), and an increased viscosity of pancreatic juice (eg,
diuretics and steroids) [37,38].

Drug-induced pancreatitis is classified (class I-IV) based on the number of cases

reported, demonstration of a consistent latency period (time from initiation of drug
to development of pancreatitis), and reaction with rechallenge (table 1) [39]. Class
I and II drugs have the greatest potential for causing acute pancreatitis (table 2).
However, proving the association with a particular drug may not always be
straightforward, even in suspected cases. Pancreatitis may develop within a few
weeks after beginning a drug associated with an immunologically mediated
adverse reaction; in this setting, the patient may also have a rash and eosinophilia.
In contrast, patients taking valproic acid, pentamidine, or didanosine may not
develop pancreatitis until after many months of use, presumably due to the
chronic accumulation of toxic metabolic products. Thus, patients restarted on
their medications should be closely monitored and the drug promptly discontinued
if symptoms recur.

Pancreatic duct injury — Blunt or penetrating trauma can damage the pancreas,

however, these injuries are uncommon due to the retroperitoneal location of the
pancreas [40,41]. Trauma can range from a mild contusion to a severe crush injury
or transection of the gland where the pancreas crosses over the spine. Pancreatin
injury can cause acute duct rupture and pancreatic ascites. Healing of pancreatic
ductal injuries can lead to scarring and stricture of the main pancreatic duct, with
resultant obstructive pancreatitis in the gland downstream from the stricture.

Other rare causes

Biliary sludge and microlithiasis — Biliary sludge is a viscous suspension in

gallbladder bile that may contain small stones (<5 mm in diameter) [42].
Microscopic analysis of bile in patients with sludge often shows cholesterol
monohydrate crystals or calcium bilirubinate granules [43]. Sludge is typically
found in patients with functional or mechanical bile stasis, such as those
undergoing a prolonged fast, with distal bile duct obstruction, or on total
parenteral nutrition. Most patients with biliary sludge are asymptomatic. However,
biliary sludge is found in 20 to 40 percent of patients with acute pancreatitis with
no obvious cause. In the absence of any other etiology, biliary sludge should be
suspected as the cause in patients with acute pancreatitis with a transient
elevation in liver tests. (See 'Recurrent episodes' below.)

Biliary obstruction — Conditions causing obstruction of the ampulla that have

been associated with pancreatitis include biliary ascariasis, periampullary
diverticula, and pancreatic and periampullary tumors [44-46]. Autoimmune
pancreatitis is a rare cause of acute pancreatitis; its usual presentation is weight
loss, jaundice, and pancreatic enlargement on imaging, mimicking a neoplasm. In
rare cases, duodenal inflammation and papillary stenosis secondary to celiac
disease can cause recurrent episodes of acute pancreatitis [47]. (See
"Autoimmune pancreatitis" and "Intraductal papillary mucinous neoplasm of the
pancreas (IPMN): Pathophysiology and clinical manifestations".)

Hypercalcemia — Hypercalcemia of any cause can lead to acute pancreatitis

but the incidence is low [48,49]. Proposed mechanisms include deposition of
calcium in the pancreatic duct and calcium activation of trypsinogen within the
pancreatic parenchyma [48-51]. The low incidence of pancreatitis in patients with
chronic hypercalcemia suggests that other factors (acute rise in serum calcium)
are responsible in patients who develop acute pancreatitis [52]. An experimental
model, for example, found that acute calcium infusions in rats led to
hyperamylasemia and dose-dependent morphological alterations characteristic of
acute pancreatitis [50]. (See "Etiology of hypercalcemia".)

Infections and toxins — Pancreatitis has been associated with the following

infections [53,54]:

● Viruses – Mumps, coxsackievirus, hepatitis B, cytomegalovirus, varicella-

zoster, herpes simplex, human immunodeficiency virus (HIV)

● Bacteria – Mycoplasma, Legionella, Leptospira, Salmonella

● Fungi – Aspergillus

● Parasites – Toxoplasma, Cryptosporidium, Ascaris

There are limited data regarding the frequency with which these infections lead to
pancreatitis. In one series, acute pancreatitis occurred in 4.7 percent of 939
hospitalized patients who were seropositive for HIV [55]. Acute pancreatitis may
be part of primary HIV infection but more frequently occurs as a complication of
medications taken to treat the virus (eg, didanosine) or opportunistic infections
(eg, pentamidine), or due to the opportunistic infection itself (eg, Pneumocystis
carinii, Mycobacterium avium-intracellulare) [54,56].

Only 70 percent of individuals have a characteristic syndrome caused by the

infectious agent [53]. In addition, the value of treating the infectious agent to
reverse pancreatitis remains unknown. Thus, the routine search for an infectious
etiology in idiopathic pancreatitis is not recommended.

The venom of arachnids and reptiles (brown recluse spider, some scorpions, and
the Gila monster lizard) have been associated with acute pancreatitis due to
cholinergic stimulation. (See "Scorpion envenomation causing autonomic
dysfunction (North Africa, Middle East, Asia, South America, and the Republic of
Trinidad and Tobago)", section on 'Pancreatitis'.)

Vascular disease — Pancreatic ischemia is an uncommon cause of clinically

significant pancreatitis. Ischemia with resultant pancreatitis has been reported in
association with vasculitis (systemic lupus erythematosus and polyarteritis
nodosa), atheroembolism, intraoperative hypotension, and hemorrhagic shock [57-
61]. A porcine model of cardiogenic shock induced by pericardial tamponade
found that pancreatic vasospasm was responsible for significant selective
pancreatic ischemia [62].

Most patients have mild attacks of pancreatitis secondary to ischemia, although

fatal necrotizing pancreatitis can occur. In one report, for example, 81 of 300
patients (27 percent) undergoing cardiac surgery developed hyperamylasemia and
three patients subsequently developed necrotizing pancreatitis [60]. Preoperative
renal insufficiency, postoperative hypotension, and perioperative administration of
calcium chloride were significant risk factors for the development of pancreatitis.

Anatomic or physiologic pancreatic anomalies — Biliary cysts (eg, some

choledochal cysts types) may increase the risk for acute pancreatitis, presumably
due to pressure and obstruction of pancreatic duct or anomalous
pancreaticobiliary malunion with a long common channel. Other anatomic
anomalies like pancreaticobiliary malunion, large juxta-ampullary diverticula, and
annular pancreas have also been associated with acute pancreatitis, possibly due
to mechanical obstruction at the ampullary level. (See "Biliary cysts", section on
'Types of biliary cysts'.)

Whether sphincter of Oddi dysfunction or pancreas divisum are a cause of acute

pancreatitis is controversial. (See "Pancreas divisum: Clinical manifestations and
diagnosis".)
Idiopathic — No obvious etiology is identifiable by history, laboratory tests, and
gallbladder ultrasound in 25 to 30 percent of patients with acute pancreatitis. After
an extensive work-up for recurrent pancreatitis (including magnetic resonance
imaging/magnetic resonance cholangiopancreatography, endoscopic ultrasound,
endoscopic retrograde cholangiopancreatography, analysis of bile for
microlithiasis, and sphincter of Oddi manometry), approximately 15 to 25 percent
of patients with acute pancreatitis are idiopathic. Emerging data indicates that the
majority of patients with idiopathic acute and recurrent acute pancreatitis have
underlying complex genetic risk profiles [63,64].

APPROACH TO ESTABLISHING THE UNDERLYING ETIOLOGY

The etiology of acute pancreatitis can be established in nearly 75 percent of

patients [14].

Initial evaluation

History — Key elements to the history include the following:

● Prior symptoms of gallstone disease (eg, biliary colic) or documentation of

gallstones on prior imaging.

● Systemic symptoms including unexplained weight loss or new onset of

diabetes.

● Amount and pattern of alcohol use. Alcoholic pancreatitis is unlikely to be the

underlying etiology in the absence of a history of over five years of heavy
alcohol consumption (>50 g per day).

● Medication use (prescription and nonprescription) including the time course

of developing pancreatitis and the presence of associated symptoms (rash
eosinophilia). (See 'Medications' above.)
 ● Prior surgery, endoscopic retrograde cholangiopancreatography (ERCP), or
trauma.

● History of hypertriglyceridemia or hypercalcemia.

● Concomitant autoimmune diseases suggestive of autoimmune pancreatitis.

● Family history of recurrent acute pancreatitis, idiopathic chronic pancreatitis,

childhood pancreatitis without a known cause and pancreatic cancer. (See
'Genetic risk' above.)

Laboratory evaluation

Routine tests in all patients — Routine tests in all patients with acute

pancreatitis should include the following:

● Triglyceride levels – Serum triglyceride levels >1000 mg/dL (11.2 mmol/L)

are required for hypertriglyceridemia to be considered the underlying etiology
of acute pancreatitis. Hypertriglyceridemia may be missed if levels are
obtained after prolonged fasting. Fasting triglyceride levels should therefore
be rechecked once the patient has resumed a normal diet. (See
"Hypertriglyceridemia-induced acute pancreatitis".)

● Serum calcium levels – Hypercalcemia may be missed during a severe attack

because calcium levels can decrease. Calcium levels should be re-checked
after few weeks of recovery, as is the case with triglycerides. However,
hypercalcemia is an unusual cause of acute pancreatitis. Other causes should
be excluded before concluding that hypercalcemia is the underlying etiology.

● Liver biochemical tests – The presence of elevated liver tests (alanine

aminotransferase [ALT] or aspartate aminotransferase [AST]) in the setting of
acute pancreatitis is suggestive of gallstone/biliary pancreatitis [65]. In one
meta-analysis, a serum ALT concentration of 150 international units/L or more
(approximately a threefold elevation) had a positive predictive value of 95
 percent for the diagnosis of gallstone pancreatitis. The AST concentration
was nearly as useful as, ALT, while the total bilirubin and alkaline phosphatase
concentrations did not assist in making the diagnosis.

Additional tests in selected patients

● In patients with acute pancreatitis at a young age (<35 years) or a family

history of pancreatitis, we perform genetic testing for hereditary pancreatitis
(eg, PRSS1, SPINK1, CFTR, CTRC and CASR and Claudin-2, if available). (See
'Genetic risk' above.)

● We do not routinely perform serologic testing for IgG4. Although autoimmune

pancreatitis (AIP) can present with acute pancreatitis it is rare. AIP is also an
extremely unlikely cause of recurrent acute pancreatitis. Serologic testing is
not an important diagnostic feature, and if AIP is suspected, then the
diagnosis is largely based on imaging, other organ involvement, and histology,
if available. (See "Autoimmune pancreatitis", section on 'Diagnosis'.)

Abdominal ultrasound — An abdominal ultrasound should be obtained on

admission in all patients with acute pancreatitis to evaluate for cholelithiasis or
choledocholithiasis or signs of extrahepatic biliary tract obstruction. The
ultrasound should be performed regardless of whether liver tests are elevated.

If the initial examination is inadequate or if clinical suspicion for gallstones

remains high, the abdominal ultrasound examination should be repeated after
recovery. (See "Management of acute pancreatitis", section on 'Gallstone
pancreatitis'.)

Subsequent evaluation for acute pancreatitis without a clear etiology — In

patients with acute pancreatitis without a clear etiology despite initial testing,
additional evaluation is required to identify other causes that may be missed
during the initial evaluation.
Although pancreatic cancer is a rare cause of acute pancreatitis, it should be
suspected in patients with acute pancreatitis who are older than 40 years of age,
have unexplained weight loss preceding the attack of acute pancreatitis, new
onset of diabetes, or a family history of pancreatic cancer in first-degree relative.

Isolated episode — In patients with an isolated episode of acute pancreatitis

without a clear etiology we perform an endoscopic ultrasonography (EUS) to
evaluate for pancreatic ductal abnormalities, small tumors at or near the ampulla,
microlithiasis in the gallbladder or bile duct, and early chronic pancreatitis.

We perform magnetic resonance cholangiopancreatography (MRCP) with secretin

administration if the EUS does not reveal a cause or is unavailable. MRCP may
sometimes unmask a dynamic obstruction or early chronic pancreatitis that may
have been rarely missed on EUS. Computed tomography with pancreas protocol
should be performed if MRCP and EUS are unavailable.

ERCP is not routinely recommended as a diagnostic test for idiopathic acute

pancreatitis because of its complications. It is reserved for endotherapy in
patients with abnormal MRCP/EUS findings (eg, choledocholithiasis, and
pancreatic ductal stricture), to diagnose a small tumor in the terminal bile duct or
pancreatic duct in patients with a suspected pancreatic neoplasm, to perform
intraductal endoscopy in patients with a main duct intraductal papillary mucinous
neoplasm.

Recurrent episodes — In patients with recurrent episodes of acute pancreatitis

we perform an EUS. We collect bile for microscopic evaluation for cholesterol or
bilirubinate crystals if EUS imaging is negative, especially if there is a strong
suspicion for biliary pancreatitis (eg, due to elevated ALT). The bile sample is
collected during the same endoscopic session as the EUS. (See "Overview of
gallstone disease in adults", section on 'Bile microscopy' and 'Laboratory
evaluation' above and 'Biliary sludge and microlithiasis' above.)
We perform MRCP with secretin administration if the EUS and bile microscopy
does not reveal a cause or are unavailable. In patients with abnormal MRCP/EUS,
ERCP is performed to confirm the diagnosis and/or endotherapy. In patients with
normal MRCP and EUS, but recurrent episodes of pancreatitis (regardless of age),
some experts perform ERCP to measure biliary and pancreatic pressures to
evaluate for sphincter of Oddi dysfunction or to perform biliary and or pancreatic
sphincterotomies, regardless of such measurements. However, it is important to
note that there is significant controversy about whether sphincter of Oddi
dysfunction is an underlying cause of idiopathic recurrent acute pancreatitis.
Sphincterotomy has also not been demonstrated to reduce the risk of acute
pancreatitis in patients with sphincter of Oddi dysfunction [66]. In addition, both
ERCP and sphincter of Oddi manometry are associated with procedure-related
complications. If ERCP is performed, it should only be performed by an
endoscopist with experience in pancreatic endotherapy. (See "Clinical
manifestations and diagnosis of sphincter of Oddi dysfunction" and "Pancreas
divisum: Clinical manifestations and diagnosis".)

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries

and regions around the world are provided separately. (See "Society guideline
links: Acute pancreatitis".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and
"Beyond the Basics." The Basics patient education pieces are written in plain
language, at the 5th to 6th grade reading level, and they answer the four or five key
questions a patient might have about a given condition. These articles are best for
patients who want a general overview and who prefer short, easy-to-read
materials. Beyond the Basics patient education pieces are longer, more
sophisticated, and more detailed. These articles are written at the 10th to 12th
grade reading level and are best for patients who want in-depth information and
are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We
encourage you to print or e-mail these topics to your patients. (You can also locate
patient education articles on a variety of subjects by searching on "patient info"
and the keyword(s) of interest.)

● Basics topics (see "Patient education: Pancreatitis (The Basics)")

● Beyond the Basics topics (see "Patient education: Acute pancreatitis (Beyond
the Basics)")

SUMMARY AND RECOMMENDATIONS

● Acute pancreatitis is an inflammatory condition of the pancreas characterized
clinically by abdominal pain and elevated levels of pancreatic enzymes in the
blood. The reported annual incidence of acute pancreatitis in the United
States ranges from 4.9 to 35 per 100,000 population. (See 'Introduction'
above.)

● A number of conditions are known to cause acute pancreatitis. Of these,

gallstones and chronic alcohol abuse account for approximately two-thirds of
cases. Gallstones (including microlithiasis) are the most common cause of
acute pancreatitis, however, only 3 to 7 percent of patients with gallstones
develop pancreatitis. (See 'Gallstones' above and 'Alcohol' above.)

● Initial evaluation to determine the etiology of acute pancreatitis, includes a

history, laboratory evaluation (serum amylase or lipase, triglyceride level,
 calcium level, and liver biochemistries), and abdominal ultrasound (repeated,
if initially negative for gallstones). (See 'Initial evaluation' above.)

In patients with acute pancreatitis at a young age (<35 years) or a family

history of pancreatitis, we perform genetic testing for hereditary pancreatitis
(eg, PRSS1, SPINK1, CFTR, CTRC, CASR and Claudin-2). (See 'Additional tests in
selected patients' above and 'Initial evaluation' above.)

● In patients with an isolated episode of acute pancreatitis, if the initial

evaluation does not yield an etiology, we perform an endoscopic
ultrasonography (EUS). In patients with a negative EUS or if EUS is
unavailable, we perform magnetic resonance cholangiopancreatography
(MRCP) following secretin administration. Endoscopic retrograde
cholangiopancreatography (ERCP) is not routinely recommended as a
diagnostic test for idiopathic acute pancreatitis because of its complications.
It is reserved for endotherapy in patients with abnormal MRCP/EUS findings
(eg, choledocholithiasis, and pancreatic ductal stricture), to diagnose a small
tumor in the terminal bile duct or pancreatic duct in patients with a suspected
pancreatic neoplasm, or to perform intraductal endoscopy in patients with a
main duct intraductal papillary mucinous neoplasm. (See 'Isolated episode'
above.)

● In patients with recurrent episodes of pancreatitis (irrespective of age), EUS is

the preferred initial test. We collect bile for microscopic evaluation for
cholesterol or bilirubinate crystals if EUS imaging is negative. We perform
MRCP following secretin administration in patients with a negative EUS and
bile microscopy. We do not routinely perform ERCP unless indicated for
additional evaluation of abnormal MRCP/EUS findings or endotherapy. There
is significant controversy about whether sphincter of Oddi dysfunction is an
underlying cause of idiopathic recurrent acute pancreatitis and both ERCP
 and sphincter of Oddi manometry are associated with procedure-related
complications. (See 'Recurrent episodes' above.)

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