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Chronic Pancreatitis

Patients with prior acute pancreatitis are susceptible to recurrent episodes due to either chronic toxic insults or genetic susceptibility. Repeated pancreatic parenchymal injury and chronic inflammation result in fibrosis. Fibrosis involving the pancreatic ducts leads to duct strictures with proximal duct dilatation. Calculi form secondary to stasis of secretions and calcification of protein plugs. Ductal obstruction and repeated injury lead to parenchymal loss and pancreatic atrophy. Loss of acinar cells results in pancreatic exocrine insufficiency which causes maldigestion, steatorrhea, weight loss, and fat-soluble vitamin deficiencies.

Chronic pancreatitis is most commonly caused by excessive alcohol use, smoking, or genetic mutations. Alcohol abuse is the most common etiology of CP and is diagnosed in 42% to 77% of patients. Smoking is associated with risk of CP in a dose-dependent fashion. Between 28% to 80% of patients are classified as having idiopathic chronic pancreatitis. Up to 50% of idiopathic cases have mutations of the serine protease inhibitor Kazal type 1 (SPINK1) gene, cystic fibrosis transmembrane conductance regulator (CFTR) gene or chymotrypsin C (CTRC) gene. Approximately 1% of people diagnosed with CP may have hereditary pancreatitis, associated with autosomal dominant inheritance of cationic trypsinogen 1 (PRSS1) gene mutations.

Genetic mutations can cause cellular injury and chronic pancreatitis in a trypsin dependent or independent manner. Mutations may lead to premature or increased activation of trypsinogen due to either gain-of-function variants in the cationic trypsinogen gene (PRSS1) or loss-of-function variants in genes such as SPINK1 and chymotrypsin C (CTRC) that code for trypsin inactivating proteins. Trypsin-independent mutations in CFTR, carboxypeptidase A1 (CPA1), and claudin 2 genes cause cellular injury by different mechanisms. Cystic fibrosis transmembrane conductance regulator dysfunction most likely affects bicarbonate secretion by the pancreatic ductal cell.

Contrast-enhanced computed tomographic (CT) scan is the best initial diagnostic test for chronic pancreatitis. Clinical laboratory tests are less useful. Amylase and lipase are helpful for diagnosing acute pancreatitis but not chronic pancreatitis. The 72-hour fecal fat test is the classical test for steatorrhea but lacks specificity for pancreatic exocrine insufficiency because it cannot differentiate between different causes of fat malabsorption. It is less popular today because it so difficult to collect and perform properly. Measurement of fecal elastase is an alternative indicator of pancreatic insufficiency. A fecal elastase concentration below 100 ug per g of stool is considered to represent severe exocrine insufficiency. At this cutoff, sensitivity is 88% and specificity is 82%. No criteria have been established for mild to moderate exocrine insufficiency.


Singh VK, Yadav D, Promod KG. Diagnosis and Management of Chronic Pancreatitis: A Review. JAMA. 2019;322(24):2422-2434

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