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Chronic pancreatitis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: : Iqra Qamar M.D.[2]

Synonyms and keywords: Pancreatitis, chronic;

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Iqra Qamar M.D.[2]

Overview

Chronic pancreatitis is a long-standing inflammatory disease of the pancreas characterized by irreversible changes in pancreatic structure and function leading to inflammation and fibrosis. The concept of pancreas and pancreatic duct was first described by Johannes Wirsung of Padua in 1642. The classification systems that have been used up til now for chronic pancreatitis include; Marseille, Marseille-Rome, Cambridge, TIGAR-O, ABC grading system, and Manchester system. The pathogenesis is still unclear and multifactorial but decreased bicarbonate secretion and intrapancreatic activation of digestive enzymes is thought to play an important role in the pathogenesis of chronic pancreatitis. Other factors that are thought to play an important role in the pathogenesis of chronic pancreatitis may include intraductal plugging and obstruction, direct injury to pancreatic cells induced by toxins and toxic metabolites, antioxidants, ischemia, autoimmune disorders, the sentinal acute pancreatitis event (SAPE) hypothesis, necrosis and fibrosis. Genes involved in the pathogenesis of chronic pancreatitis include CFTR-cystic fibrosis gene mutation, SPINK-1, which encodes for trypsin inhibitor, PRSS-1 gene linked to hereditary pancreatitis, claudin-2 (CLDN2), and carboxypeptidase A1 (CPA1) genes. TIGAR-O may be used for the etiologic classification of chronic pancreatitis. Chronic pancreatitis needs to be differentiated from other diseases presenting with similar complaints such as abdominal pain, diarrhea, and weight loss. The incidence of chronic pancreatitis and the number of hospital admissions secondary to chronic pancreatitis is increasing in most countries worldwide. Alcoholic pancreatitis is more prevalent in developed or industrialized countries. Idiopathic and tropical pancreatitis is more prevalent in developing and underdeveloped countries. The M-ANNHEIM multiple risk factor classification of chronic pancreatitis includes multiple risk factors such as alcohol consumption, nicotine consumption, nutritional factors, hereditary factors, efferent duct factors, immunological factors, rare metabolic factors, and miscellaneous factors. The risk of progression of chronic pancreatitis to pancreatic cancer is approximately 4% at 20 years. Common complications of chronic pancreatitis usually include pseudocyst formation and mechanical obstruction of the duodenum and common bile duct. The diagnostic study of choice for chronic pancreatitis is magnetic resonance cholangiopancreatography (MRCP). The diagnosis is difficult to establish as the laboratory results and the imaging may be normal. Patients with chronic pancreatitis usually present with persistent abdominal pain with episodic flares that may or may not be associated with food intake, steatorrhea, pancreatic diabetes, nausea and weight loss. A secretin stimulation test is considered the gold standard functional test for diagnosis of chronic pancreatitis. Fecal tests may include sudan staining of feces, 72-hour quantitative fecal fat (gold standard), and faecal elastase measurement (test of choice). CT scan findings suggestive of chronic pancreatitis may include dilatation of the main pancreatic duct, calcifications, pancreatic gland enlargement, changes in pancreatic size, shape, and contour, and pancreatic pseudocysts. MRI findings may include parenchymal atrophy or enlargement, pseudocyst formation, dilatation and beading of the pancreatic duct with intraductal calcifications giving an appearance of ‘chain of lakes’. ERCP findings diagnostic of chronic pancreatitis may include beaded appearance of the main pancreatic duct and ectatic side branches from the main pancreatic duct. Presence of stones is the most predictive finding seen on endoscopic ultrasonography. Other diagnostic studies may include genetic testing such as CFTR-Cystic fibrosis gene mutation, SPINK-1, which encodes for trypsin inhibitor and PRSS-1 gene linked to hereditary pancreatitis. Medical therapy includes pancreatic enzyme supplementation, analgesics and antioxidants. Specialized approaches include celiac nerve block, endoscopic therapy, extracorporeal shock wave lithotripsy (ESWL), and radiation. Steatorrhea can be managed by dietary modification, lipase supplementation, vitamin supplementation, and medium chain triglycerides (MCTs). Surgery for chronic pancreatitis tends to be divided into two resectional and drainage procedures. Dilated pancreatic duct may be managed with lateral pancreaticojejunostomy (LPJ) and lateral pancreaticojejunostomy with localized pancreatic head resection. Nondilated pancreatic duct is usually manages with pancreaticoduodenectomy, duodenal-preserving pancreatic head resection (DPPHR), distal pancreatectomy (DP) and total pancreatectomy (TP).

Historical Perspective

The concept of pancreas and pancreatic duct was first described by Johannes Wirsung of Padua in 1642. In 1761, Giovanni Morgagni described the clinical syndrome of severe upper abdominal pain, vomiting, and collapse. He is also credited with the earliest pathological recognition of cancer of the pancreas. In 1948, Eliason and Welty described distal pancreatectomy (DP). In 1980, Beger described duodenal-preserving pancreatic head resection (DPPHR) technique for chronic pancreatitis to decrease the morbidity of pancreatic head resection.

Classification

Chronic pancreatitis may be divided based upon underlying morphology into large-duct type or small-duct type with or without calcification. The classification systems that have been used up til now for chronic pancreatitis may include ; Marseille, Marseille-Rome, Cambridge, TIGAR-O, ABC grading system and Manchester system.

Pathophysiology

Chronic pancreatitis is a progressive inflammatory process leading to irreversible structural damage to pancreas resulting in exocrine and endocrine dysfunction. The pathogenesis is still unclear and multifactorial but decreased bicarbonate secretion and intrapancreatic activation of digestive enzymes is thought to play an important role in the pathogenesis of chronic pancreatitis. Other factors that are thought to play an important role in the pathogenesis of chronic pancreatitis may include intraductal plugging and obstruction, direct injury to pancreatic cells induced by toxins and toxic metabolites, antioxidants, ischemia, autoimmune disorders, the sentinal acute pancreatitis event (SAPE) hypothesis, necrosis and fibrosis. Genes involved in the pathogenesis of chronic pancreatitis include CFTR-cystic fibrosis gene mutation, SPINK-1, which encodes for trypsin inhibitor, PRSS-1 gene linked to hereditary pancreatitis, claudin-2 (CLDN2), and carboxypeptidase A1 (CPA1) genes. Associated conditions may include autoimmune conditions, primary biliary cirrhosis, primary sclerosing cholangitis, sjögren syndrome, and renal tubular acidosis. Gross pathology may include enlarged or atrophic pancreas, cysts, calcifications, fibrosis and patchy focal necrosis. Microscopic histopathological analysis may show patchy focal disease characterized by a mononuclear infiltrate.

Causes

TIGAR-O may be used for the etiologic classification of chronic pancreatitis. Toxic causes may include alcohol, tobacco smoking, hypercalcemia, hyperlipidemia, chronic renal failure, medications, and toxins. Genetic causes of chronic pancreatitis may include cationic trypsinogen (PRSS1), cystic fibrosis transmembrane conductance regulator gene (CFTR), calcium-sensing receptor (CASR), chymotrypsin C gene (CTRC) and pancreatic secretory trypsin inhibitor gene (SPINK1). Less common causes may include hypertriglyceridemia, scorpion sting, tropical pancreatitis and medications such as metronidazole, ercaptopurine, valproate, isoniazid and corticosteroids.

Differentiating Chronic pancreatitis overview from Other Diseases

Chronic pancreatitis needs to be differentiated from other diseases presenting with similar complaints such as abdominal pain, diarrhea and weight loss.

Epidemiology and Demographics

The incidence of chronic pancreatitis and the number of hospital admissions is increasing in most countries worldwide. The incidence of chronic pancreatitis is approximately 1.6 to 23 cases per 100,000 individuals per year worldwide. A rising level of per capita alcohol consumption is correlated with an increasing prevalence of chronic pancreatitis. Changes in lifestyle modifications such as smoking and alcohol cessation may result in slowing the progression and reducing the incidence of chronic pancreatitis. Alcoholic pancreatitis is more prevalent in developed or industrialized countries. Idiopathic and tropical pancreatitis is more prevalent in developing and underdeveloped countries.

Risk Factors

The M-ANNHEIM multiple risk factor classification of chronic pancreatitis includes multiple risk factors, alcohol consumption, nicotine consumption, nutritional factors, hereditary factors, efferent duct factors, immunological factors, miscellaneous and rare metabolic factors. Common risk factors may include alcohol abuse, cigarette smoking, genetic mutations (PRSS1 mutations, SPINK1 mutations, CFTR mutations, and CTRC mutations), obstructive causes and hypercalcemia. Less common risk factors may include sphincter of Oddi dysfunction, hyperlipidemia, metabolic diseases such as branched-chain organic aciduria, and chronic renal failure.

Screening

Patients with chronic pancreatitis should be screened for diabetes annually and should be followed up with fasting glucose and HbA1c levels.

Natural History, Complications, and Prognosis

The natural history of pain is highly variable and mostly involves intermittent pain attacks that decrease or resolve over 5-25 years while a few patients may have chronic pain. The risk of progression of chronic pancreatitis to pancreatic cancer is approximately 4% at 20 years. Common complications usually include pseudocyst and mechanical obstruction of the duodenum and common bile duct. Less common complications may include pancreatic ascites, pleural effusion, pseudoaneurysm formation, and splenic vein thrombosis. Prognostic factors associated with chronic pancreatitis may include the age at diagnosis, smoking status, continued use of alcohol, and presence of liver cirrhosis. In chronic pancreatitis, the overall survival rate is 70% at 10 years and the 10-year mortality rate is 30%.

Diagnosis

Diagnostic study of choice:

The diagnostic study of choice for chronic pancreatitis is magnetic resonance cholangiopancreatography (MRCP). The diagnosis is difficult to establish as the laboratory results and the imaging may be normal. Diagnostic findings confirmatory for chronic pancreatitis may include pancreatic calcifications seen on abdominal plain films or CT scan, beaded appearance of main pancreatic duct seen on pancreatogram, abnormal pancreatogram showing ecstatic side branches from the main pancreatic duct and abnormal pancreatic function tests (Secretin test).

Diagnostic criteria:

The M-ANNHEIM diagnostic criteria for chronic pancreatitis can be used to identify and differentiate various forms of chronic pancreatitis. M-ANNHEIM pancreatic imaging criteria for US, CT, MRI/MRCP, and EUS based on imaging features as defined by the Cambridge classification includes normal, equivocal, mild, moderate and marked changes.

History and Symptoms:

Patients with chronic pancreatitis usually present with persistent abdominal pain with episodic flares that may or may not be associated with food intake steatorrhea, pancreatic diabetes, nausea, and weight loss. According to M-ANNHEIM clinical staging of chronic pancreatitis, it can be classified into asymptomatic and symptomatic chronic pancreatitis. M-ANNHEIM scoring system for the grading of clinical features of chronic pancreatitis include features such as pain control, surgical intervention, exocrine insufficiency, endocrine insufficiency, morphologic status on pancreatic imaging and severe organ complications.

Physical Examination:

Patients with chronic pancreatitis may assume a characteristic position in an attempt to relieve their abdominal pain such as lying on the left side, flexing the spine, drawing the knees up toward the chest. Patients with steatorrhea or advanced disease may present as loss of subcutaneous fat, temporal wasting and sunken supraclavicular fossa. Skin findings may include jaundice, pallor, and bruises.

Laboratory Findings:

The diagnosis of chronic pancreatitis is typically based on tests on pancreatic structure and function. Serum amylase and lipase are usually normal but may be slightly elevated. Serum calcium and triglyceride levels may be elevated in hypertriglyceridemia induced pancreatitis. A secretin stimulation test is considered the gold standard functional test for diagnosis of chronic pancreatitis. Fecal tests may include sudan staining of feces, 72-hour quantitative fecal fat (gold standard), and faecal elastase measurement (test of choice).

Abdominal X-ray:

An x-ray may be helpful in the diagnosis of chronic pancreatitis. Finding on an x-ray suggestive of chronic pancreatitis includes pancreatic calcification.

CT scan:

CT scan findings suggestive of chronic pancreatitis may include dilatation of the main pancreatic duct, calcifications, pancreatic gland enlargement, changes in pancreatic size, shape, contour, and pancreatic pseudocysts. Contrast enhanced CT scan may be helpful in ruling out other diseases with similar presentation such as malignancy and pseudocysts. The sensitivity of CT scan is 75 to 90 percent and specificity is 85 percent.

MRI:

MRI findings for chronic pancreatitis may be classified as early and late findings. Early findings may include low-signal-intensity pancreas on T1-weighted fat-suppressed images, decreased and delayed enhancement after IV contrast administration and dilated side branches. Late findings may include parenchymal atrophy or enlargement, pseudocyst formation, dilatation and beading of the pancreatic duct with intraductal calcifications giving an appearance of ‘chain of lakes’.

Ultrasound:

Ultrasound findings suggestive of chronic pancreatitis may include dilatation of the main pancreatic duct, calcifications, pancreatic gland enlargement, changes in pancreatic size, shape, and contour, pancreatic pseudocysts, hyperechogenicity suggesting fibrotic changes, pseudoaneurysms and ascites. The sensitivity of ultrasound is 60 to 70 percent and the specificity of ultrasound is 80 to 90 percent. The pancreas might appear atrophic, calcified or fibrotic (advanced stages).

Other imaging findings:

Other imaging findings may include MRCP, ERCP, and endoscopic ultrasonography. MRCP is the diagnostic study of choice. MRCP findings suggestive of chronic pancreatitis may include calcifications and pancreatic duct obstruction. ERCP findings diagnostic of chronic pancreatitis may include beaded appearance of the main pancreatic duct and ectatic side branches from the main pancreatic duct. Presence of stones is the most predictive finding seen on endoscopic ultrasonography. Other findings suggestive of chronic pancreatitis may include visible side branches, cysts, lobularity, an irregular main pancreatic duct, hyperechoic foci, dilation of the main pancreatic duct and hyperechoic margins of the main pancreatic duct. Pancreatic function tests may include direct tests such as secretin stimulation tests and indirect tests.

Other diagnostic studies:

Other diagnostic studies may include genetic testing such as CFTR-cystic fibrosis gene mutation, SPINK-1, which encodes for trypsin inhibitor and PRSS-1 gene linked to hereditary pancreatitis. Routine genetic testing is usually not recommended for CFTR and SPINK-1 genes as it is expensive, do not alter the management and false positive results.

Treatment

Medical Therapy

The goals of chronic pancreatitis management include pain control, management of pancreatic insufficiency by pancreatic enzyme replacement and management of complications. Pain is managed in a stepwise approach of general recommendations, pancreatic enzyme replacement, analgesics and invasive procedures. General recommendations usually include smoking cessation, cessation of alcohol intake, small meals and hydration. Medical therapy includes pancreatic enzyme supplementation, analgesics and antioxidants. Specialized approaches include celiac nerve block, endoscopic therapy, extracorporeal shock wave lithotripsy (ESWL), and radiation. Steatorrhea can be managed by dietary modification, lipase supplementation, vitamin supplementation, and medium chain triglycerides (MCTs). Diabetes is usually managed with a trial of oral hypoglycemic agents followed by insulin therapy.

Surgery

Surgery is usually considered when pain management fails with medical and endoscopic therapies. The goals of surgery include effective pain relief, and to preserve long-term pancreatic function. Surgery for chronic pancreatitis tends to be divided into two areas – resectional and drainage procedures. Dilated pancreatic duct may be managed with lateral pancreaticojejunostomy (LPJ) and lateralpancreaticojejunostomy with localized pancreatic head resection. Nondilated pancreatic duct is usually managed with pancreaticoduodenectomy, duodenal-preserving pancreatic head resection (DPPHR), distal pancreatectomy (DP) and total pancreatectomy (TP).

Primary Prevention

Secondary Prevention

Effective measures for the secondary prevention of Hereditary pancreatitis include low-fat diet, multiple small meals, good hydration, antioxidants and cessation/abstinence from smoking and alcohol use. Patients should be managed appropriately and timely with glucocorticoids and immunomodulatory drugs to prevent complications.

References


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Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Iqra Qamar M.D.[2]

Overview

The concept of pancreas and pancreatic duct was first described by Johannes Wirsung of Padua in 1642. In 1761, Giovanni Morgagni described the clinical syndrome of severe upper abdominal pain, vomiting, and collapse as the presentation of chronic pancreatitis. He is also credited with the earliest recognition of cancer of the pancreas. In 1948, Eliason and Welty described distal pancreatectomy (DP). In 1980, Beger described duodenum-preserving pancreatic head resection (DPPHR) technique for chronic pancreatitis to decrease the morbidity of pancreatic head resection.

Historical Perspective

The historical landmarks in the diagnostic evaluation and management of acute pancreatitis are as follows:[1][2]

  • In 1642, Johannes Wirsung of Padua first described the pancreatic duct and the concept of the pancreas as a secretory organ.
  • In 1652, Nicholaes Tulp was credited with the first description of acute pancreatitis.
  • In 1737, Giovanni Santorini of Venice identified a second, accessory duct and was credited with the discovery of the ampulla of Vater.
  • In 1887, Rugero Oddi published his observations on the structure and function of the choledochal sphincter in “Archives Italiennes de Biologie”, that laid the basis for understanding its role in pancreatic and biliary disease.
  • In the 16th century, Sylvius Franciscus de la Boe Sylvius found that the pancreas discharges a fluid that mixes with the partly digested food and bile in the intestine causing an effervescence (“effervescentia intestinalis”) which liquefies food.
  • In the 16th century, Regnier de Graaf of Delft devised novel surgical techniques to create pancreatic fistulas (center) to collect this juice for analysis.
  • In 1761, Giovanni Morgagni described the clinical syndrome of severe upper abdominal pain, vomiting, and collapse. He is also credited with the earliest recognition of cancer of the pancreas.
  • In 1842, Karl von Rokitansky, the premier pathologist of Vienna (Wiener Allgemeines Krankenhaus) was the first one to recognize acute hemorrhagic pancreatitis.
  • In late 18th century, Reginald Fitz described 3 forms of acute pancreatitis (hemorrhagic, suppurative, and gangrenous) and proposed that fat necrosis is a consequence of severe pancreatitis.
  • In late 18th century, Nicholas Senn of Chicago, not only addressed the mechanisms behind acute pancreatitis but also provided rational insight into the validity of surgical techniques for its treatment.
  • In 1948, Eliason and Welty described distal pancreatectomy (DP).[3]
  • In 1980, Beger described duodenum-preserving pancreatic head resection (DPPHR) technique for chronic pancreatitis to decrease the morbidity of pancreatic head resection.[4][5][6][4][7][8]

References

  1. ↑ Pannala R, Kidd M, Modlin IM (2009). “Acute pancreatitis: a historical perspective”. Pancreas. 38 (4): 355–66. doi:10.1097/MPA.0b013e318199161c. PMID 19390402.
  2. ↑ Fitz, Reginald H. (1889). “Acute Pancreatitis”. The Boston Medical and Surgical Journal. 120 (8): 181–187. doi:10.1056/NEJM188902211200801. ISSN 0096-6762.
  3. ↑ Eliason EL, Welty RF (1948). “Pancreatic Calculi”. Ann. Surg. 127 (1): 150–7. PMC 1513761. PMID 17859057.
  4. ↑ 4.0 4.1 Beger HG, Schlosser W, Friess HM, Büchler MW (1999). “Duodenum-preserving head resection in chronic pancreatitis changes the natural course of the disease: a single-center 26-year experience”. Ann. Surg. 230 (4): 512–9, discussion 519–23. PMC 1420900. PMID 10522721.
  5. ↑ Klempa I, Spatny M, Menzel J, Baca I, Nustede R, Stöckmann F, Arnold W (1995). “[Pancreatic function and quality of life after resection of the head of the pancreas in chronic pancreatitis. A prospective, randomized comparative study after duodenum preserving resection of the head of the pancreas versus Whipple’s operation]”. Chirurg (in German). 66 (4): 350–9. PMID 7634946.
  6. ↑ Beger HG, Krautzberger W, Bittner R, Büchler M, Limmer J (1985). “Duodenum-preserving resection of the head of the pancreas in patients with severe chronic pancreatitis”. Surgery. 97 (4): 467–73. PMID 3983823.
  7. ↑ Beger HG, Büchler M, Bittner RR, Oettinger W, Roscher R (1989). “Duodenum-preserving resection of the head of the pancreas in severe chronic pancreatitis. Early and late results”. Ann. Surg. 209 (3): 273–8. PMC 1493931. PMID 2923514.
  8. ↑ Büchler MW, Friess H, Bittner R, Roscher R, Krautzberger W, Müller MW, Malfertheiner P, Beger HG (1997). “Duodenum-preserving pancreatic head resection: Long-term results”. J. Gastrointest. Surg. 1 (1): 13–9. PMID 9834325.


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Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Iqra Qamar M.D.[2]

Overview

Chronic pancreatitis may be divided based upon underlying morphology into large-duct type or small-duct type with or without calcification. The classification systems that have been used for chronic pancreatitis include Marseille, Marseille-Rome system, Cambridge system, TIGAR-O system, ABC grading system and Manchester system.

Classification

Classification based upon morphology

Chronic pancreatitis may be divided based on underlying morphology into:

Classification system for chronic pancreatitis Year Key features
Clinical description 1946
  • Description of the clinical presentation of chronic pancreatitis and its association with increased alcohol consumption
Marseille 1963
  • Description of morphologic characteristics and etiological factors of the disease
  • No discussion of the correlation between anatomic and functional changes
  • No categorization according to disease severity or clinical presentation
  • No inclusion of pancreatic imaging findings
Marseille 1984
  • Further description and subclassification of morphological changes
  • “Obstructive chronic pancreatitis” listed as distinct form
  • No discussion of the correlation between anatomic and functional changes
  • No categorization according to disease severity or clinical presentation
  • No inclusion of pancreatic imaging findings
Marseille-Rome 1988
  • Description of “chronic calcifying” and “chronic inflammatory” pancreatitis as distinct forms
  • Description of etiological factors
  • No further elaboration of clinical, functional or imaging criteria
Cambridge 1984
Clinical stages 1994
  • Detailed subclassification of chronic pancreatitis with correlation of etiological factors with different morphological forms of the disease
  • Differentiation of clinical stages of the disease
  • Linkage of pancreatic imaging findings and functional testing with stages of the disease
Japan Pancreas Society 1997
  • Description of clinical presentation and classification of disease in “definite” and “probable” chronic pancreatitis according to imaging findings, functional testing, and histological examination
Zürich Workshop 1997
  • Description of clinical presentation and classification of disease in “definite” and “probable” chronic pancreatitis according to imaging findings, functional testing, and histological examination
TIGAR-O 2001
ABC grading system 2002
  • Disease grading according to clinical criteria, but limited separation of different disease severities
  • Not all clinical presentations can be categorized
Manchester system 2006
  • Disease grading according to clinical criteria, but limited separation of different disease severities
  • Not all clinical presentations can be categorized

Classification of pancreatitis based upon area of involvement and etiology

There are various forms of chronic pancreatitis based upon the area of involvement and etiology are as follows:

Groove pancreatitis:

Groove pancreatitis is a form of segmental pancreatitis that involves confinement of the inflammation process to the groove between the duodenum, common bile duct, and head of the pancreas without any involvement of the head of pancreas.[1]

Hereditary pancreatitis:

Autoimmune pancreatitis (AIP):

Tropical pancreatitis:

  • Tropical pancreatitis is one of the most common causes of chronic pancreatitis in tropical areas including south India.
  • It was thought to be caused by cassava fruit but no longer associated with it and has no clear etiology.[3]
  • It usually affects children leading to early adulthood death due to endocrine and exocrine dysfunction.
  • Serine protease inhibitor SPINK1 mutations are identified in some of the patients.[4][5]

Idiopathic pancreatitis:

References

  1. ↑ Tezuka K, Makino T, Hirai I, Kimura W (2010). “Groove pancreatitis”. Dig Surg. 27 (2): 149–52. doi:10.1159/000289099. PMID 20551662.
  2. ↑ Sossenheimer MJ, Aston CE, Preston RA, Gates LK, Ulrich CD, Martin SP, Zhang Y, Gorry MC, Ehrlich GD, Whitcomb DC (1997). “Clinical characteristics of hereditary pancreatitis in a large family, based on high-risk haplotype. The Midwest Multicenter Pancreatic Study Group (MMPSG)”. Am. J. Gastroenterol. 92 (7): 1113–6. PMID 9219780.
  3. ↑ Sarles H, Augustine P, Laugier R, Mathew S, Dupuy P (1994). “Pancreatic lesions and modifications of pancreatic juice in tropical chronic pancreatitis (tropical calcific diabetes)”. Dig. Dis. Sci. 39 (6): 1337–44. PMID 8200268.
  4. ↑ Bhatia E, Choudhuri G, Sikora SS, Landt O, Kage A, Becker M, Witt H (2002). “Tropical calcific pancreatitis: strong association with SPINK1 trypsin inhibitor mutations”. Gastroenterology. 123 (4): 1020–5. PMID 12360463.
  5. ↑ Schneider A, Suman A, Rossi L, Barmada MM, Beglinger C, Parvin S, Sattar S, Ali L, Khan AK, Gyr N, Whitcomb DC (2002). “SPINK1/PSTI mutations are associated with tropical pancreatitis and type II diabetes mellitus in Bangladesh”. Gastroenterology. 123 (4): 1026–30. PMID 12360464.

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Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Iqra Qamar M.D.[2]


Overview

Chronic pancreatitis is a progressive inflammatory process leading to irreversible structural damage to the pancreas resulting in exocrine and endocrine dysfunction. The pathogenesis is still unclear and multifactorial. Decreased bicarbonate secretion and intrapancreatic activation of digestive enzymes is thought to play an important role in the pathogenesis of chronic pancreatitis. Other factors that are thought to play an important role in the pathogenesis of chronic pancreatitis may include intraductal plugging and obstruction, direct injury to pancreatic cells induced by toxins and toxic metabolites, antioxidants, ischemia, autoimmune disorders, the sentinal acute pancreatitis event (SAPE), necrosis and fibrosis. Genes involved in the pathogenesis of chronic pancreatitis include CFTR-cystic fibrosis gene mutation, SPINK-1 mutation, which encodes for trypsin inhibitor, PRSS-1 gene mutation linked to hereditary pancreatitis, claudin-2 (CLDN2), and carboxypeptidase A1 (CPA1) gene mutations. Associated conditions may include autoimmune conditions, primary biliary cirrhosis, primary sclerosing cholangitis, Sjögren syndrome, and renal tubular acidosis. Gross pathology may include enlarged or atrophic pancreas, cysts, calcifications, fibrosis and patchy focal necrosis. Microscopic histopathological analysis may show patchy focal disease characterized by a mononuclear infiltrate.

Pathophysiology

Chronic pancreatitis is a progressive inflammatory process leading to irreversible structural damage to the pancreas resulting in exocrine and endocrine dysfunction.[1] The pathogenesis is still unclear and multifactorial; but two mechanisms that play an important role in the pathogenesis of chronic pancreatitis, which are as follows:

Decreased bicarbonate secretion:

A decrease in bicarbonate secretion may be due to any of the following causes:

  • Protein hypersecretion resulting in proteinaceous ductal plugs leading to ductal blockage and obstruction[2]

Intrapancreatic activation of digestive enzymes:

By Robert Jaster [CC BY 2.0 (http://creativecommons.org/licenses/by/2.0)], via Wikimedia Commons

Other factors that are thought to play an important role in the pathogenesis of chronic pancreatitis include:

(a) Intraductal plugging and obstruction

1) Proteinaceous ductal plugs
2) Intraductal obstruction due to other causes

(b) Direct injury to pancreatic cells induced by toxins and toxic metabolites

(c) Antioxidants

(d) Ischemia

(e) Autoimmune disorders

(f) Necrosis and fibrosis

(g) The sentinal acute pancreatitis event (SAPE) hypothesis:

Source: nih.gov

Genetics

Genes involved in the pathogenesis of chronic pancreatitis include:

Associated Conditions

Gross Pathology

By Dr. Roshan Nasimudeen [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)], via Wikimedia Commons
By Dr. Roshan Nasimudeen [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)], via Wikimedia Commons
Case courtesy of Dr Henry Knipe, <a href="https://radiopaedia.org/">Radiopaedia.org</a>. From the case <a href="https://radiopaedia.org/cases/27870">rID: 27870</a>
Case courtesy of Dr Henry Knipe, <a href=”https://radiopaedia.org/“>Radiopaedia.org</a>. From the case <a href=”https://radiopaedia.org/cases/27870“>rID: 27870</a>

Microscopic Pathology

Type Uneven pancreatic lipomatosis
Type 1a Preferential fatty replacement of head
Type 1b Preferential fatty replacement of head, neck and body
Type 2a Preferential fatty replacement of head and uncinate process
Type 2b Fatty replacement of most of pancreas except peribiliary region
By Patho – Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=29668664
By Patho – Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=29668789

Staging according to pancreatic physiology:

Stage Pancreatic physiology
A Normal secretory, exocrine, and endocrine function
B Secretory dysfunction (abnormal secretin stimulation test)
C Exocrine insufficiency (abnormal fecal elastase, steatorrhea, low serum trypsin)
D Endocrine insufficiency (abnormal fasting glucose, glycohemoglobin, glucose tolerance test)
E Both C & D
X Not classified/ unknown

References

  1. ↑ Steer ML, Waxman I, Freedman S (1995). “Chronic pancreatitis”. N. Engl. J. Med. 332 (22): 1482–90. doi:10.1056/NEJM199506013322206. PMID 7739686.
  2. ↑ 2.0 2.1 Sahel J, Sarles H (1979). “Modifications of pure human pancreatic juice induced by chronic alcohol consumption”. Dig. Dis. Sci. 24 (12): 897–905. PMID 510088.
  3. ↑ Freedman SD, Sakamoto K, Venu RP (1993). “GP2, the homologue to the renal cast protein uromodulin, is a major component of intraductal plugs in chronic pancreatitis”. J. Clin. Invest. 92 (1): 83–90. doi:10.1172/JCI116602. PMC 293537. PMID 8326020.
  4. ↑ Guy O, Robles-Diaz G, Adrich Z, Sahel J, Sarles H (1983). “Protein content of precipitates present in pancreatic juice of alcoholic subjects and patients with chronic calcifying pancreatitis”. Gastroenterology. 84 (1): 102–7. PMID 6401181.
  5. ↑ Apte MV, Pirola RC, Wilson JS (2010). “Mechanisms of alcoholic pancreatitis”. J Gastroenterol Hepatol. 25 (12): 1816–26. doi:10.1111/j.1440-1746.2010.06445.x. PMID 21091991.
  6. ↑ Forsmark CE, Vege SS, Wilcox M (November 17,2016). “Acute Pancreatitis”. The New England Journal of Medicine: 1972–1981. doi:10.1056/NEJMra1505202. Retrieved November 25,2016. Check date values in: |access-date=, |date= (help)
  7. ↑ Rose P, Fraine E, Hunt LP, Acheson DW, Braganza JM (1986). “Dietary antioxidants and chronic pancreatitis”. Hum Nutr Clin Nutr. 40 (2): 151–64. PMID 3957720.
  8. ↑ Uden S, Acheson DW, Reeves J, Worthington HV, Hunt LP, Brown S, Braganza JM (1988). “Antioxidants, enzyme induction, and chronic pancreatitis: a reappraisal following studies in patients on anticonvulsants”. Eur J Clin Nutr. 42 (7): 561–9. PMID 3224602.
  9. ↑ Braganza JM, Thomas A, Robinson A (1988). “Antioxidants to treat chronic pancreatitis in childhood? Case report and possible implications for pathogenesis”. Int. J. Pancreatol. 3 (2–3): 209–16. doi:10.1007/BF02798933. PMID 3361161.
  10. ↑ Bhardwaj P, Garg PK, Maulik SK, Saraya A, Tandon RK, Acharya SK (2009). “A randomized controlled trial of antioxidant supplementation for pain relief in patients with chronic pancreatitis”. Gastroenterology. 136 (1): 149–159.e2. doi:10.1053/j.gastro.2008.09.028. PMID 18952082.
  11. ↑ Burton F, Alkaade S, Collins D, Muddana V, Slivka A, Brand RE, Gelrud A, Banks PA, Sherman S, Anderson MA, Romagnuolo J, Lawrence C, Baillie J, Gardner TB, Lewis MD, Amann ST, Lieb JG, O’Connell M, Kennard ED, Yadav D, Whitcomb DC, Forsmark CE (2011). “Use and perceived effectiveness of non-analgesic medical therapies for chronic pancreatitis in the United States”. Aliment. Pharmacol. Ther. 33 (1): 149–59. doi:10.1111/j.1365-2036.2010.04491.x. PMC 3142582. PMID 21083584.
  12. ↑ Karanjia ND, Singh SM, Widdison AL, Lutrin FJ, Reber HA (1992). “Pancreatic ductal and interstitial pressures in cats with chronic pancreatitis”. Dig. Dis. Sci. 37 (2): 268–73. PMID 1735346.
  13. ↑ Tanaka T, Ichiba Y, Miura Y, Ito H, Dohi K (1994). “Canine model of chronic pancreatitis due to chronic ischemia”. Digestion. 55 (2): 86–9. PMID 7514552.
  14. ↑ Epstein O, Chapman RW, Lake-Bakaar G, Foo AY, Rosalki SB, Sherlock S (1982). “The pancreas in primary biliary cirrhosis and primary sclerosing cholangitis”. Gastroenterology. 83 (6): 1177–82. PMID 7129026.
  15. ↑ Nishimori I, Yamamoto Y, Okazaki K, Morita M, Onodera M, Kino J, Tamura S, Yamamoto Y (1994). “Identification of autoantibodies to a pancreatic antigen in patients with idiopathic chronic pancreatitis and Sjögren’s syndrome”. Pancreas. 9 (3): 374–81. PMID 8022761.
  16. ↑ Bovo P, Mirakian R, Merigo F, Angelini G, Cavallini G, Rizzini P, Bottazzo GF, Scuro LA (1987). “HLA molecule expression on chronic pancreatitis specimens: is there a role for autoimmunity? A preliminary study”. Pancreas. 2 (3): 350–6. PMID 3498162.
  17. ↑ 17.0 17.1 Schneider A, Whitcomb DC (2002). “Hereditary pancreatitis: a model for inflammatory diseases of the pancreas”. Best Pract Res Clin Gastroenterol. 16 (3): 347–63. doi:10.1053/bega.2002.0311. PMID 12079262.
  18. ↑ Lankisch PG, Breuer N, Bruns A, Weber-Dany B, Lowenfels AB, Maisonneuve P (2009). “Natural history of acute pancreatitis: a long-term population-based study”. Am. J. Gastroenterol. 104 (11): 2797–805, quiz 2806. doi:10.1038/ajg.2009.405. PMID 19603011.
  19. ↑ Ammann RW, Muellhaupt B (1994). “Progression of alcoholic acute to chronic pancreatitis”. Gut. 35 (4): 552–6. PMC 1374808. PMID 8174996.
  20. ↑ Yadav D, Whitcomb DC (2010). “The role of alcohol and smoking in pancreatitis”. Nat Rev Gastroenterol Hepatol. 7 (3): 131–45. doi:10.1038/nrgastro.2010.6. PMID 20125091.
  21. ↑ Bishop MD, Freedman SD, Zielenski J, Ahmed N, Dupuis A, Martin S, Ellis L, Shea J, Hopper I, Corey M, Kortan P, Haber G, Ross C, Tzountzouris J, Steele L, Ray PN, Tsui LC, Durie PR (2005). “The cystic fibrosis transmembrane conductance regulator gene and ion channel function in patients with idiopathic pancreatitis”. Hum. Genet. 118 (3–4): 372–81. doi:10.1007/s00439-005-0059-z. PMID 16193325.
  22. ↑ Ooi CY, Gonska T, Durie PR, Freedman SD (2010). “Genetic testing in pancreatitis”. Gastroenterology. 138 (7): 2202–6, 2206.e1. doi:10.1053/j.gastro.2010.04.022. PMID 20416310.
  23. ↑ Witt H, Luck W, Hennies HC, Classen M, Kage A, Lass U, Landt O, Becker M (2000). “Mutations in the gene encoding the serine protease inhibitor, Kazal type 1 are associated with chronic pancreatitis”. Nat. Genet. 25 (2): 213–6. doi:10.1038/76088. PMID 10835640.
  24. ↑ Whitcomb DC, LaRusch J, Krasinskas AM, Klei L, Smith JP, Brand RE, Neoptolemos JP, Lerch MM, Tector M, Sandhu BS, Guda NM, Orlichenko L, Alkaade S, Amann ST, Anderson MA, Baillie J, Banks PA, Conwell D, Coté GA, Cotton PB, DiSario J, Farrer LA, Forsmark CE, Johnstone M, Gardner TB, Gelrud A, Greenhalf W, Haines JL, Hartman DJ, Hawes RA, Lawrence C, Lewis M, Mayerle J, Mayeux R, Melhem NM, Money ME, Muniraj T, Papachristou GI, Pericak-Vance MA, Romagnuolo J, Schellenberg GD, Sherman S, Simon P, Singh VP, Slivka A, Stolz D, Sutton R, Weiss FU, Wilcox CM, Zarnescu NO, Wisniewski SR, O’Connell MR, Kienholz ML, Roeder K, Barmada MM, Yadav D, Devlin B (2012). “Common genetic variants in the CLDN2 and PRSS1-PRSS2 loci alter risk for alcohol-related and sporadic pancreatitis”. Nat. Genet. 44 (12): 1349–54. doi:10.1038/ng.2466. PMC 3510344. PMID 23143602.
  25. ↑ Witt H, Beer S, Rosendahl J, Chen JM, Chandak GR, Masamune A, Bence M, Szmola R, Oracz G, Macek M, Bhatia E, Steigenberger S, Lasher D, Bühler F, Delaporte C, Tebbing J, Ludwig M, Pilsak C, Saum K, Bugert P, Masson E, Paliwal S, Bhaskar S, Sobczynska-Tomaszewska A, Bak D, Balascak I, Choudhuri G, Nageshwar Reddy D, Rao GV, Thomas V, Kume K, Nakano E, Kakuta Y, Shimosegawa T, Durko L, Szabó A, Schnúr A, Hegyi P, Rakonczay Z, Pfützer R, Schneider A, Groneberg DA, Braun M, Schmidt H, Witt U, Friess H, Algül H, Landt O, Schuelke M, Krüger R, Wiedenmann B, Schmidt F, Zimmer KP, Kovacs P, Stumvoll M, Blüher M, Müller T, Janecke A, Teich N, Grützmann R, Schulz HU, Mössner J, Keim V, Löhr M, Férec C, Sahin-Tóth M (2013). “Variants in CPA1 are strongly associated with early onset chronic pancreatitis”. Nat. Genet. 45 (10): 1216–20. doi:10.1038/ng.2730. PMC 3909499. PMID 23955596.


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Causes

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Iqra Qamar M.D.[2]

Overview

TIGAR-O (toxic metabolite, idiopathic, genetic, autoimmune, recurrent and acute, obstructive) classification system may be used for the etiologic classification of chronic pancreatitis. Toxic causes may include use of alcohol, tobacco smoking, hypercalcemia, hyperlipidemia, chronic renal failure, medications, and toxins. Genetic causes may include cationic trypsinogen gene (PRSS1) mutation, cystic fibrosis transmembrane conductance regulator (CFTR) gene mutation, calcium-sensing receptor (CASR) gene mutation, chymotrypsin C (CTRC) gene mutation, and mutation in the pancreatic secretory trypsin inhibitor gene (SPINK1). Less common causes may include hypertriglyceridemia, scorpion sting, tropical pancreatitis, and medications such as metronidazole, mercaptopurine, valproate, isoniazid and corticosteroids.

Causes

TIGAR-O (toxic metabolite, idiopathic, genetic, autoimmune, recurrent and acute, obstructive) etiologic classification of chronic pancreatitis includes:

Etiology Causes
Toxic-metabolic
Idiopathic
  • Early onset
  • Late onset
  • Tropical
Genetic
Autoimmune
Recurrent and severe acute pancreatitis
Obstructive

Common causes

There are many causes of chronic pancreatitis. At least 70% of adult cases are associated with chronic alcohol use, primarily in patients who consume more than 80 g/day of alcohol over six to twelve years[1][2]. Common causes of chronic pancreatitis may include:[3][4][5]

Less common causes:

References

  1. ↑ Nair RJ, Lawler L, Miller MR (2007). “Chronic pancreatitis”. Am Fam Physician. 76 (11): 1679–88. PMID 18092710.
  2. ↑ Mitchell RMS et al. Pancreatitis. Lancet 2003; 361: 1447–55
  3. ↑ Mitchell RMS et al. Pancreatitis. Lancet 2003; 361: 1447–55
  4. ↑ Frulloni et al. Chronic pancreatitis: Report from a multicenter Italian survey (PanCroInfAISP) on 893 patients. Dig Liver Dis. 2009 Apr;41(4):311-7
  5. ↑ Adsay NV et al. Paraduodenal pancreatitis: a clinico-pathologically distinct entity unifying “cystic dystrophy of heterotopic pancreas”, “para-duodenal wall cyst”, and “groove pancreatitis”. Semin Diagn Pathol. 2004 Nov;21(4):247-54.
  6. ↑ Lu Z, Karne S, Kolodecik T, Gorelick FS (2002). “Alcohols enhance caerulein-induced zymogen activation in pancreatic acinar cells”. Am. J. Physiol. Gastrointest. Liver Physiol. 282 (3): G501–7. doi:10.1152/ajpgi.00388.2001. PMC 2830557. PMID 11842000.
  7. ↑ Bisceglie AM, Segal I (1984). “Cirrhosis and chronic pancreatitis in alcoholics”. J. Clin. Gastroenterol. 6 (3): 199–200. PMID 6725910.
  8. ↑ Wilson JS, Bernstein L, McDonald C, Tait A, McNeil D, Pirola RC (1985). “Diet and drinking habits in relation to the development of alcoholic pancreatitis”. Gut. 26 (9): 882–7. PMC 1432860. PMID 4029715.
  9. ↑ Whitcomb DC (2003). “Genetic predisposition to alcoholic chronic pancreatitis”. Pancreas. 27 (4): 321–6. PMID 14576495.
  10. ↑ Maisonneuve P, Lowenfels AB, Müllhaupt B, Cavallini G, Lankisch PG, Andersen JR, Dimagno EP, Andrén-Sandberg A, Domellöf L, Frulloni L, Ammann RW (2005). “Cigarette smoking accelerates progression of alcoholic chronic pancreatitis”. Gut. 54 (4): 510–4. doi:10.1136/gut.2004.039263. PMC 1774435. PMID 15753536.
  11. ↑ Morton C, Klatsky AL, Udaltsova N (2004). “Smoking, coffee, and pancreatitis”. Am. J. Gastroenterol. 99 (4): 731–8. doi:10.1111/j.1572-0241.2004.04143.x. PMID 15089909.
  12. ↑ Coté GA, Yadav D, Slivka A, Hawes RH, Anderson MA, Burton FR, Brand RE, Banks PA, Lewis MD, Disario JA, Gardner TB, Gelrud A, Amann ST, Baillie J, Money ME, O’Connell M, Whitcomb DC, Sherman S (2011). “Alcohol and smoking as risk factors in an epidemiology study of patients with chronic pancreatitis”. Clin. Gastroenterol. Hepatol. 9 (3): 266–73, quiz e27. doi:10.1016/j.cgh.2010.10.015. PMC 3043170. PMID 21029787.
  13. ↑ Epstein O, Chapman RW, Lake-Bakaar G, Foo AY, Rosalki SB, Sherlock S (1982). “The pancreas in primary biliary cirrhosis and primary sclerosing cholangitis”. Gastroenterology. 83 (6): 1177–82. PMID 7129026.
  14. ↑ Nishimori I, Yamamoto Y, Okazaki K, Morita M, Onodera M, Kino J, Tamura S, Yamamoto Y (1994). “Identification of autoantibodies to a pancreatic antigen in patients with idiopathic chronic pancreatitis and Sjögren’s syndrome”. Pancreas. 9 (3): 374–81. PMID 8022761.
  15. ↑ Tarnasky PR, Hoffman B, Aabakken L, Knapple WL, Coyle W, Pineau B, Cunningham JT, Cotton PB, Hawes RH (1997). “Sphincter of Oddi dysfunction is associated with chronic pancreatitis”. Am. J. Gastroenterol. 92 (7): 1125–9. PMID 9219783.
  16. ↑ 16.0 16.1 Lehman GA, Sherman S (1995). “Pancreas divisum. Diagnosis, clinical significance, and management alternatives”. Gastrointest. Endosc. Clin. N. Am. 5 (1): 145–70. PMID 7728342.
  17. ↑ 17.0 17.1 Delhaye M, Engelholm L, Cremer M (1985). “Pancreas divisum: congenital anatomic variant or anomaly? Contribution of endoscopic retrograde dorsal pancreatography”. Gastroenterology. 89 (5): 951–8. PMID 4043675.
  18. ↑ 18.0 18.1 Sherman S, Hawes RH, Savides TJ, Gress FG, Ikenberry SO, Smith MT, Zaidi S, Lehman GA (1996). “Stent-induced pancreatic ductal and parenchymal changes: correlation of endoscopic ultrasound with ERCP”. Gastrointest. Endosc. 44 (3): 276–82. PMID 8885346.
  19. ↑ 19.0 19.1 Smith MT, Sherman S, Ikenberry SO, Hawes RH, Lehman GA (1996). “Alterations in pancreatic ductal morphology following polyethylene pancreatic stent therapy”. Gastrointest. Endosc. 44 (3): 268–75. PMID 8885345.
  20. ↑ Tezuka K, Makino T, Hirai I, Kimura W (2010). “Groove pancreatitis”. Dig Surg. 27 (2): 149–52. doi:10.1159/000289099. PMID 20551662.
  21. ↑ Bess MA, Edis AJ, van Heerden JA (1980). “Hyperparathyroidism and pancreatitis. Chance or a causal association?”. JAMA. 243 (3): 246–7. PMID 7350371.
  22. ↑ Masaryk TJ, Achkar E (1983). “Pancreatitis as initial presentation of cystic fibrosis in young adults. A report of two cases”. Dig. Dis. Sci. 28 (10): 874–8. PMID 6617400.
  23. ↑ Borum M, Steinberg W, Steer M, Freedman S, White P (1993). “Chronic pancreatitis: a complication of systemic lupus erythematosus”. Gastroenterology. 104 (2): 613–5. PMID 8425705.
  24. ↑ Cohn JA, Friedman KJ, Noone PG, Knowles MR, Silverman LM, Jowell PS (1998). “Relation between mutations of the cystic fibrosis gene and idiopathic pancreatitis”. N. Engl. J. Med. 339 (10): 653–8. doi:10.1056/NEJM199809033391002. PMID 9725922.
  25. ↑ Sharer N, Schwarz M, Malone G, Howarth A, Painter J, Super M, Braganza J (1998). “Mutations of the cystic fibrosis gene in patients with chronic pancreatitis”. N. Engl. J. Med. 339 (10): 645–52. doi:10.1056/NEJM199809033391001. PMID 9725921.
  26. ↑ Bishop MD, Freedman SD, Zielenski J, Ahmed N, Dupuis A, Martin S, Ellis L, Shea J, Hopper I, Corey M, Kortan P, Haber G, Ross C, Tzountzouris J, Steele L, Ray PN, Tsui LC, Durie PR (2005). “The cystic fibrosis transmembrane conductance regulator gene and ion channel function in patients with idiopathic pancreatitis”. Hum. Genet. 118 (3–4): 372–81. doi:10.1007/s00439-005-0059-z. PMID 16193325.
  27. ↑ Noone PG, Zhou Z, Silverman LM, Jowell PS, Knowles MR, Cohn JA (2001). “Cystic fibrosis gene mutations and pancreatitis risk: relation to epithelial ion transport and trypsin inhibitor gene mutations”. Gastroenterology. 121 (6): 1310–9. PMID 11729110.
  28. ↑ LaRusch J, Jung J, General IJ, Lewis MD, Park HW, Brand RE, Gelrud A, Anderson MA, Banks PA, Conwell D, Lawrence C, Romagnuolo J, Baillie J, Alkaade S, Cote G, Gardner TB, Amann ST, Slivka A, Sandhu B, Aloe A, Kienholz ML, Yadav D, Barmada MM, Bahar I, Lee MG, Whitcomb DC (2014). “Mechanisms of CFTR functional variants that impair regulated bicarbonate permeation and increase risk for pancreatitis but not for cystic fibrosis”. PLoS Genet. 10 (7): e1004376. doi:10.1371/journal.pgen.1004376. PMC 4102440. PMID 25033378.
  29. ↑ Witt H, Luck W, Hennies HC, Classen M, Kage A, Lass U, Landt O, Becker M (2000). “Mutations in the gene encoding the serine protease inhibitor, Kazal type 1 are associated with chronic pancreatitis”. Nat. Genet. 25 (2): 213–6. doi:10.1038/76088. PMID 10835640.
  30. ↑ Rosendahl J, Witt H, Szmola R, Bhatia E, Ozsvári B, Landt O, Schulz HU, Gress TM, Pfützer R, Löhr M, Kovacs P, Blüher M, Stumvoll M, Choudhuri G, Hegyi P, te Morsche RH, Drenth JP, Truninger K, Macek M, Puhl G, Witt U, Schmidt H, Büning C, Ockenga J, Kage A, Groneberg DA, Nickel R, Berg T, Wiedenmann B, Bödeker H, Keim V, Mössner J, Teich N, Sahin-Tóth M (2008). “Chymotrypsin C (CTRC) variants that diminish activity or secretion are associated with chronic pancreatitis”. Nat. Genet. 40 (1): 78–82. doi:10.1038/ng.2007.44. PMC 2650829. PMID 18059268.
  31. ↑ Sossenheimer MJ, Aston CE, Preston RA, Gates LK, Ulrich CD, Martin SP, Zhang Y, Gorry MC, Ehrlich GD, Whitcomb DC (1997). “Clinical characteristics of hereditary pancreatitis in a large family, based on high-risk haplotype. The Midwest Multicenter Pancreatic Study Group (MMPSG)”. Am. J. Gastroenterol. 92 (7): 1113–6. PMID 9219780.
  32. ↑ Sarles H, Augustine P, Laugier R, Mathew S, Dupuy P (1994). “Pancreatic lesions and modifications of pancreatic juice in tropical chronic pancreatitis (tropical calcific diabetes)”. Dig. Dis. Sci. 39 (6): 1337–44. PMID 8200268.
  33. ↑ Bhatia E, Choudhuri G, Sikora SS, Landt O, Kage A, Becker M, Witt H (2002). “Tropical calcific pancreatitis: strong association with SPINK1 trypsin inhibitor mutations”. Gastroenterology. 123 (4): 1020–5. PMID 12360463.
  34. ↑ Schneider A, Suman A, Rossi L, Barmada MM, Beglinger C, Parvin S, Sattar S, Ali L, Khan AK, Gyr N, Whitcomb DC (2002). “SPINK1/PSTI mutations are associated with tropical pancreatitis and type II diabetes mellitus in Bangladesh”. Gastroenterology. 123 (4): 1026–30. PMID 12360464.
  35. ↑ Cox DW, Breckenridge WC, Little JA (1978). “Inheritance of apolipoprotein C-II deficiency with hypertriglyceridemia and pancreatitis”. N. Engl. J. Med. 299 (26): 1421–4. doi:10.1056/NEJM197812282992601. PMID 213719.


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Differentiating Chronic pancreatitis from other Diseases

Differentiating Chronic pancreatitis from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Iqra Qamar M.D.[2]

Overview

Chronic pancreatitis should be differentiated from other diseases presenting with similar symptoms such as abdominal pain, diarrhea and weight loss.

Differentiating Chronic Pancreatitis from Other Diseases

Differentials based upon abdominal pain, weight loss and diarrhea:

Abbreviations: RUQ= Right upper quadrant of the abdomen, LUQ= Left upper quadrant, LLQ= Left lower quadrant, RLQ= Right lower quadrant, LFT= Liver function tests, SIRS= Systemic inflammatory response syndrome, ERCP= Endoscopic retrograde cholangiopancreatography, IV= Intravenous, N= Normal, AMA= Anti mitochondrial antibodies, LDH= Lactate dehydrogenase, GI= Gastrointestinal, CXR= Chest X ray, US= Ultrasound, IgA= Immunoglobulin A, IgG= Immunoglobulin G, IgM= Immunoglobulin M, CT= Computed tomography, PMN= Polymorphonuclear cells, ESR= Erythrocyte sedimentation rate, CRP= C-reactive protein, TS= Transferrin saturation, SF= Serum Ferritin, SMA= Superior mesenteric artery, SMV= Superior mesenteric vein, ECG= Electrocardiogram

Disease Clinical manifestations Diagnosis Comments
Symptoms Signs
Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo-

tension

Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging
Chronic pancreatitis Epigastric − − ± ± − + + − − − − N
  • Increased amylase / lipase
  • Increased stool fat content
  • Pancreatic function test
 CT scan
  • Calcification
  • Pseudocyst
  • Dilation of main pancreatic duct
  • Predisposes to pancreatic cancer
Pancreatic carcinoma Epigastric − − + + − + + − − − − N

Skin manifestations may include:

Dumping syndrome Lower and then diffuse − − + − − + + − + − − Hyperactive
  • Glucose challenge test
  • Hydrogen breath test
  • Upper GI series
  • Gastric emptying study
  • Postgastrectomy
Inflammatory bowel disease Diffuse ± − − ± − + + + − − − Normal or hyperactive

Extra intestinal findings:

Irritable bowel syndrome Diffuse − − − − ± ± + − − − − N Normal Normal Symptomatic treatment
Whipple’s disease Diffuse ± − − ± − + + − ± − − N Endoscopy is used to confirm diagnosis.

Images used to find complications

Extra intestinal findings:
Disease Abdominal Pain Fever Rigors and chills Nausea or vomiting Jaundice Constipation Diarrhea Weight loss GI bleeding Hypo-

tension

Guarding Rebound Tenderness Bowel sounds Lab Findings Imaging Comments
Tropical sprue Diffuse + − − − − + + − − − − N Barium studies:
  • Dilation and edema of mucosal folds
Celiac disease Diffuse − − − − − + + − − − − Hyperactive US:
  • Bull’s eye or target pattern
  • Pseudokidney sign
  • Gluten allergy
Colon carcinoma Diffuse/localized − − − − ± ± + + ± − −
  • Normal or hyperactive if obstruction present
  • CBC
  • Carcinoembryonic antigen (CEA)
  • Colonoscopy
  • Flexible sigmoidoscopy
  • Barium enema
  • CT colonography 
  • PILLCAM 2: A colon capsule for CRC screening may be used in patients with an incomplete colonoscopy who lacks obstruction
Viral hepatitis RUQ + − + + − Positive in Hep A and E + − Positive in fulminant hepatitis Positive in acute + N
  • Abnormal LFTs
  • Viral serology
  • US
  • Hep A and E have fecal-oral route of transmission
  • Hep B and C transmits via blood transfusion and sexual contact.
Liver abscess RUQ + + + + − ± + − + + ± Normal or hypoactive
  • US
  • CT
Mesenteric ischemia Periumbilical Positive if bowel becomes gangrenous − + − − + + + Positive if bowel becomes gangrenous Positive if bowel becomes gangrenous − Hyperactive to absent CT angiography
  • SMA or SMV thrombosis
  • Also known as abdominal angina that worsens with eating
Acute ischemic colitis Diffuse + ± + − − + + + + + + Hyperactive then absent Abdominal x-ray
  • Distension and pneumatosis

CT scan

  • Double halo appearance, thumbprinting
  • Thickening of bowel
  • May lead to shock

To review the differential diagnosis of Abdominal pain, click here.

References


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Epidemiology and Demographics

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Iqra Qamar M.D.[2]

Overview

The incidence of chronic pancreatitis and the number of hospital admissions is increasing in most countries worldwide. The incidence of chronic pancreatitis is approximately 1.6 to 23 cases per 100,000 individuals per year worldwide. A rising level of per capita alcohol consumption is correlated with an increasing prevalence of chronic pancreatitis. Changes in lifestyle modifications such as smoking and alcohol cessation may result in slowing the progression and reducing the incidence of chronic pancreatitis. Alcoholic pancreatitis is more prevalent in developed or industrialized countries. Idiopathic and tropical pancreatitis is more prevalent in developing and underdeveloped countries.

Epidemiology and Demographics

Incidence

  • In 2004, the incidence of chronic pancreatitis was estimated to be 8.1 per 100,000 individuals in the United States of America.[1]
  • The incidence of chronic pancreatitis is approximately 1.6 to 23 cases per 100,000 individuals per year worldwide.
  • In United States, chronic pancreatitis results in:
    • >122,000 outpatient visits per year.
    • >56,000 hospitalizations per year.
  • The incidence of chronic pancreatitis and the number of hospital admissions is increasing in most countries worldwide.
  • Changes in lifestyle modifications such as smoking and alcohol cessation may result in slowing the progression and reducing the incidence of chronic pancreatitis.

Prevalence

  • A rising level of per capita alcohol consumption is correlated with an increasing prevalence of chronic pancreatitis.

Age

Gender

  • Men and women are almost equally affected in the United States.[1][7][8]
  • Men are more commonly affected by chronic pancreatitis than females in almost all countries except the United States.[9][10][11][12] [13][5][6][14][15]

Developed countries

  • Alcoholic pancreatitis is more prevalent in developed or industrialized countries.

Developing countries

  • Idiopathic and tropical pancreatitis is more prevalent in developing and underdeveloped countries.

References

  1. ↑ 1.0 1.1 Yang AL, Vadhavkar S, Singh G, Omary MB (2008). “Epidemiology of alcohol-related liver and pancreatic disease in the United States”. Arch. Intern. Med. 168 (6): 649–56. doi:10.1001/archinte.168.6.649. PMID 18362258.
  2. ↑ Lévy P, Barthet M, Mollard BR, Amouretti M, Marion-Audibert AM, Dyard F (2006). “Estimation of the prevalence and incidence of chronic pancreatitis and its complications”. Gastroenterol. Clin. Biol. 30 (6–7): 838–44. PMID 16885867.
  3. ↑ Frulloni L, Gabbrielli A, Pezzilli R, Zerbi A, Cavestro GM, Marotta F, Falconi M, Gaia E, Uomo G, Maringhini A, Mutignani M, Maisonneuve P, Di Carlo V, Cavallini G (2009). “Chronic pancreatitis: report from a multicenter Italian survey (PanCroInfAISP) on 893 patients”. Dig Liver Dis. 41 (4): 311–7. doi:10.1016/j.dld.2008.07.316. PMID 19097829.
  4. ↑ Lowenfels AB, Maisonneuve P, Grover H, Gerber E, Korsten MA, Antunes MT, Marques A, Pitchumoni CS (1999). “Racial factors and the risk of chronic pancreatitis”. Am. J. Gastroenterol. 94 (3): 790–4. doi:10.1111/j.1572-0241.1999.00952.x. PMID 10086667.
  5. ↑ 5.0 5.1 Pezzilli R, Morselli-Labate AM, Fantini L, Campana D, Corinaldesi R (2007). “Assessment of the quality of life in chronic pancreatitis using Sf-12 and EORTC Qlq-C30 questionnaires”. Dig Liver Dis. 39 (12): 1077–86. doi:10.1016/j.dld.2007.06.014. PMID 17692582.
  6. ↑ 6.0 6.1 Wehler M, Nichterlein R, Fischer B, Farnbacher M, Reulbach U, Hahn EG, Schneider T (2004). “Factors associated with health-related quality of life in chronic pancreatitis”. Am. J. Gastroenterol. 99 (1): 138–46. PMID 14687155.
  7. ↑ 7.0 7.1 Whitcomb DC, Yadav D, Adam S, Hawes RH, Brand RE, Anderson MA, Money ME, Banks PA, Bishop MD, Baillie J, Sherman S, DiSario J, Burton FR, Gardner TB, Amann ST, Gelrud A, Lo SK, DeMeo MT, Steinberg WM, Kochman ML, Etemad B, Forsmark CE, Elinoff B, Greer JB, O’Connell M, Lamb J, Barmada MM (2008). “Multicenter approach to recurrent acute and chronic pancreatitis in the United States: the North American Pancreatitis Study 2 (NAPS2)”. Pancreatology. 8 (4–5): 520–31. doi:10.1159/000152001. PMC 2790781. PMID 18765957.
  8. ↑ Tao N, Sussman S, Nieto J, Tsukamoto H, Yuan JM (2003). “Demographic characteristics of hospitalized patients with alcoholic liver disease and pancreatitis in los angeles county”. Alcohol. Clin. Exp. Res. 27 (11): 1798–804. doi:10.1097/01.ALC.0000095862.30777.D9. PMID 14634496.
  9. ↑ Lankisch PG, Assmus C, Maisonneuve P, Lowenfels AB (2002). “Epidemiology of pancreatic diseases in Lüneburg County. A study in a defined german population”. Pancreatology. 2 (5): 469–77. doi:10.1159/000064713. PMID 12378115.
  10. ↑ Jaakkola M, Nordback I (1993). “Pancreatitis in Finland between 1970 and 1989”. Gut. 34 (9): 1255–60. PMC 1375465. PMID 8406164.
  11. ↑ Wang LW, Li ZS, Li SD, Jin ZD, Zou DW, Chen F (2009). “Prevalence and clinical features of chronic pancreatitis in China: a retrospective multicenter analysis over 10 years”. Pancreas. 38 (3): 248–54. doi:10.1097/MPA.0b013e31818f6ac1. PMID 19034057.
  12. ↑ Bourliere M, Barthet M, Berthezene P, Durbec JP, Sarles H (1991). “Is tobacco a risk factor for chronic pancreatitis and alcoholic cirrhosis?”. Gut. 32 (11): 1392–5. PMC 1379175. PMID 1752475.
  13. ↑ Cavallini G, Frulloni L, Pederzoli P, Talamini G, Bovo P, Bassi C, Di Francesco V, Vaona B, Falconi M, Sartori N, Angelini G, Brunori MP, Filippini M (1998). “Long-term follow-up of patients with chronic pancreatitis in Italy”. Scand. J. Gastroenterol. 33 (8): 880–9. PMID 9754738.
  14. ↑ Garg PK, Tandon RK (2004). “Survey on chronic pancreatitis in the Asia-Pacific region”. J. Gastroenterol. Hepatol. 19 (9): 998–1004. doi:10.1111/j.1440-1746.2004.03426.x. PMID 15304116.
  15. ↑ Balakrishnan V, Unnikrishnan AG, Thomas V, Choudhuri G, Veeraraju P, Singh SP, Garg P, Pai CG, Devi RN, Bhasin D, Jayanthi V, Premalatha N, Chacko A, Kar P, Rai RR, Rajan R, Subhalal N, Mehta R, Mishra SP, Dwivedi M, Vinayakumar KR, Jain AK, Biswas K, Mathai S, Varghese J, Ramesh H, Alexander T, Philip J, Raj VV, Vinodkumar A, Mukevar S, Sawant P, Nair P, Kumar H, Sudhindran S, Dhar P, Sudheer OV, Sundaram KR, Tantri BV, Singh D, Nath TR (2008). “Chronic pancreatitis. A prospective nationwide study of 1,086 subjects from India”. JOP. 9 (5): 593–600. PMID 18762690.


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Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Iqra Qamar M.D.[2]

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Overview

The M-ANNHEIM multiple risk factor classification of chronic pancreatitis includes multiple risk factors such as alcohol consumption, nicotine consumption, nutritional factors, hereditary factors, efferent duct factors, immunological factors, miscellaneous and rare metabolic factors. Common risk factors may include alcohol abuse, cigarette smoking, genetic mutations (PRSS1 mutations, SPINK1 mutations, CFTR mutations, and CTRC mutations), obstructive causes and hypercalcemia. Less common risk factors include sphincter of Oddi dysfunction, hyperlipidemia, metabolic diseases such as branched-chain organic aciduria and chronic renal failure.

Risk Factors

The M-ANNHEIM multiple risk factor classification of chronic pancreatitis

Risk factor Sub-category
Multiple risk factors
Alcohol consumption
  • Excessive consumption (>80 g/day)
  • Increased consumption (20–80 g/day)
  • Moderate consumption (<20 g/day)
Nicotine consumption
Nutritional factors
Hereditary factors
  • Hereditary pancreatitis
  • Familial pancreatitis
  • Early-onset idiopathic pancreatitis
  • Late-onset idiopathic pancreatitis
  • Tropical pancreatitis (possible mutations in the PRSS1, CFTR, or SPINK1 genes)
Efferent duct factors
Immunological Factors
Miscellaneous and rare metabolic factors

Common risk factors

Common risk factors in the development of chronic pancreatitis include:

Less common risk factors

Less common risk factors in the development of chronic pancreatitis include:

References

  1. ↑ Lu Z, Karne S, Kolodecik T, Gorelick FS (2002). “Alcohols enhance caerulein-induced zymogen activation in pancreatic acinar cells”. Am. J. Physiol. Gastrointest. Liver Physiol. 282 (3): G501–7. doi:10.1152/ajpgi.00388.2001. PMC 2830557. PMID 11842000.
  2. ↑ Bisceglie AM, Segal I (1984). “Cirrhosis and chronic pancreatitis in alcoholics”. J. Clin. Gastroenterol. 6 (3): 199–200. PMID 6725910.
  3. ↑ Wilson JS, Bernstein L, McDonald C, Tait A, McNeil D, Pirola RC (1985). “Diet and drinking habits in relation to the development of alcoholic pancreatitis”. Gut. 26 (9): 882–7. PMC 1432860. PMID 4029715.
  4. ↑ Whitcomb DC (2003). “Genetic predisposition to alcoholic chronic pancreatitis”. Pancreas. 27 (4): 321–6. PMID 14576495.
  5. ↑ Maisonneuve P, Lowenfels AB, Müllhaupt B, Cavallini G, Lankisch PG, Andersen JR, Dimagno EP, Andrén-Sandberg A, Domellöf L, Frulloni L, Ammann RW (2005). “Cigarette smoking accelerates progression of alcoholic chronic pancreatitis”. Gut. 54 (4): 510–4. doi:10.1136/gut.2004.039263. PMC 1774435. PMID 15753536.
  6. ↑ Morton C, Klatsky AL, Udaltsova N (2004). “Smoking, coffee, and pancreatitis”. Am. J. Gastroenterol. 99 (4): 731–8. doi:10.1111/j.1572-0241.2004.04143.x. PMID 15089909.
  7. ↑ Coté GA, Yadav D, Slivka A, Hawes RH, Anderson MA, Burton FR, Brand RE, Banks PA, Lewis MD, Disario JA, Gardner TB, Gelrud A, Amann ST, Baillie J, Money ME, O’Connell M, Whitcomb DC, Sherman S (2011). “Alcohol and smoking as risk factors in an epidemiology study of patients with chronic pancreatitis”. Clin. Gastroenterol. Hepatol. 9 (3): 266–73, quiz e27. doi:10.1016/j.cgh.2010.10.015. PMC 3043170. PMID 21029787.
  8. ↑ Yadav D, Hawes RH, Brand RE, Anderson MA, Money ME, Banks PA, Bishop MD, Baillie J, Sherman S, DiSario J, Burton FR, Gardner TB, Amann ST, Gelrud A, Lawrence C, Elinoff B, Greer JB, O’Connell M, Barmada MM, Slivka A, Whitcomb DC (2009). “Alcohol consumption, cigarette smoking, and the risk of recurrent acute and chronic pancreatitis”. Arch. Intern. Med. 169 (11): 1035–45. doi:10.1001/archinternmed.2009.125. PMID 19506173.
  9. ↑ Bourliere M, Barthet M, Berthezene P, Durbec JP, Sarles H (1991). “Is tobacco a risk factor for chronic pancreatitis and alcoholic cirrhosis?”. Gut. 32 (11): 1392–5. PMC 1379175. PMID 1752475.
  10. ↑ Tarnasky PR, Hoffman B, Aabakken L, Knapple WL, Coyle W, Pineau B, Cunningham JT, Cotton PB, Hawes RH (1997). “Sphincter of Oddi dysfunction is associated with chronic pancreatitis”. Am. J. Gastroenterol. 92 (7): 1125–9. PMID 9219783.


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Screening

Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Iqra Qamar M.D.[2]

Overview

Patients with chronic pancreatitis should be screened for diabetes annually and should be followed up with fasting glucose and HbA1c levels.

Screening

Patients with chronic pancreatitis should be screened for diabetes annually via the following:[1]

References

  1. ↑ Rickels MR, Bellin M, Toledo FG, Robertson RP, Andersen DK, Chari ST, Brand R, Frulloni L, Anderson MA, Whitcomb DC (2013). “Detection, evaluation and treatment of diabetes mellitus in chronic pancreatitis: recommendations from PancreasFest 2012”. Pancreatology. 13 (4): 336–42. doi:10.1016/j.pan.2013.05.002. PMC 3830751. PMID 23890130.

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Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Iqra Qamar M.D.[2]

Overview

The natural history of chronic pacreatitis is highly variable and mostly involves episodic abdominal pain that decreases or resolves over 5-25 years, while a few patients may have chronic pain. The risk of progression of chronic pancreatitis to pancreatic cancer is approximately 4% at 20 years. Common complications usually include pseudocyst formation and mechanical obstruction of the duodenum, and common bile duct. Less common complications may include pancreatic ascites, pleural effusion, pseudoaneurysm formation, and splenic vein thrombosis. Prognostic factors affecting patients suffering from chronic pancreatitis may include the age at diagnosis, smoking history, continued use of alcohol and, presence of liver cirrhosis. In chronic pancreatitis, the overall survival rate is 70% at 10 years and the 10-year mortality rate is 30%.

Natural History

  • The natural history of chronic pancreatitis is highly variable and mostly involves episodic abdominal pain that decreases or resolves over 5-25 years, while a few patients may have chronic pain.
  • The average duration from the onset of symptoms until the establishment of the diagnosis of chronic pancreatitis in alcoholics is 62 months and 81 months in non-alcoholics.
  • In alcohol-induced pancreatitis, the pain severity may be reduced by cessation of alcohol intake.
  • The risk of progression of chronic pancreatitis to pancreatic cancer is approximately 4% at 20 years.

Complications

Prognosis

  • Prognostic factors associated with chronic pancreatitis may include:

References

  1. ↑ Rickels MR, Bellin M, Toledo FG, Robertson RP, Andersen DK, Chari ST, Brand R, Frulloni L, Anderson MA, Whitcomb DC (2013). “Detection, evaluation and treatment of diabetes mellitus in chronic pancreatitis: recommendations from PancreasFest 2012”. Pancreatology. 13 (4): 336–42. doi:10.1016/j.pan.2013.05.002. PMC 3830751. PMID 23890130.
  2. ↑ Runyon BA (1987). “Amylase levels in ascitic fluid”. J. Clin. Gastroenterol. 9 (2): 172–4. PMID 2437177.
  3. ↑ Gómez-Cerezo J, Barbado Cano A, Suárez I, Soto A, Ríos JJ, Vázquez JJ (2003). “Pancreatic ascites: study of therapeutic options by analysis of case reports and case series between the years 1975 and 2000”. Am. J. Gastroenterol. 98 (3): 568–77. PMID 12650789.
  4. ↑ Forsmark CE, Wilcox CM, Grendell JH (1992). “Endoscopy-negative upper gastrointestinal bleeding in a patient with chronic pancreatitis”. Gastroenterology. 102 (1): 320–9. PMID 1727767.
  5. ↑ Sakorafas GH, Sarr MG, Farley DR, Farnell MB (2000). “The significance of sinistral portal hypertension complicating chronic pancreatitis”. Am. J. Surg. 179 (2): 129–33. PMID 10773149.
  6. ↑ Bernades P, Baetz A, Lévy P, Belghiti J, Menu Y, Fékété F (1992). “Splenic and portal venous obstruction in chronic pancreatitis. A prospective longitudinal study of a medical-surgical series of 266 patients”. Dig. Dis. Sci. 37 (3): 340–6. PMID 1735356.
  7. ↑ Beattie GC, Hardman JG, Redhead D, Siriwardena AK (2003). “Evidence for a central role for selective mesenteric angiography in the management of the major vascular complications of pancreatitis”. Am. J. Surg. 185 (2): 96–102. PMID 12559436.
  8. ↑ Arnaud JP, Bergamaschi R, Serra-Maudet V, Casa C (1994). “Pancreatoduodenectomy for hemosuccus pancreaticus in silent chronic pancreatitis”. Arch Surg. 129 (3): 333–4. PMID 8129612.
  9. ↑ Wagner WH, Cossman DV, Treiman RL, Foran RF, Levin PM, Cohen JL (1994). “Hemosuccus pancreaticus from intraductal rupture of a primary splenic artery aneurysm”. J. Vasc. Surg. 19 (1): 158–64. PMID 8301728.
  10. ↑ Lowenfels AB, Maisonneuve P, DiMagno EP, Elitsur Y, Gates LK, Perrault J, Whitcomb DC (1997). “Hereditary pancreatitis and the risk of pancreatic cancer. International Hereditary Pancreatitis Study Group”. J. Natl. Cancer Inst. 89 (6): 442–6. PMID 9091646.


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Diagnosis

Diagnosis

Diagnostic Study of Choice | History and Symptoms | Physical Examination | Laboratory Findings | Abdominal X Ray | CT | MRI | Ultrasound | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1

Related Chapters

Template:Gastroenterology it:Pancreatite cronica fi:Krooninen haimatulehdus



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  1. ↑ <https://en.wikipedia.org/wiki/Pancreas#/media/File:Blausen_0699_PancreasAnatomy2.png>

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