Chronic pancreatitis

Chronic pancreatitis
Updated: 03/25/2019
© Jun Wang, MD, PhD

General features
  • Continuing, chronic, inflammatory process
  • Irreversible loss of pancreatic parenchyma and replacement with fibrosis
  • Variable pancreatic insufficiency (malabsorption, diabetes)
  • More common in men, 40+ years of age, alcoholics
  • May simulate or coexist with pancreatic carcinoma
  • Complications: Pseudocysts; widespread fat necrosis (from liberation of lipase), localized portal hypertension due to fibrosis of splenic vein in alcoholic hepatitis
Etiology
  • Commonly idiopathic
  • Alcohol: most common etiology (60-70%)
  • Intraductal plugging and obstruction: Stones, tumors
  • Toxins and toxic metabolites: Promotes release of cytokines
  • Oxidative stress: Idiopathic pancreatitis
  • Necrosis-fibrosis: Recurrent acute pancreatitis that heals with fibrosis
  • Ischemia: From obstruction and fibrosis; important in exacerbating disease
Pathogenesis
  • Destruction of pancreatic tissue due to recurrent inflammation
  • Fibrosis induced by TGF-beta, PDGF, etc
Clinical presentations
  • Precipitated by alcohol, overeating, opiates, other drugs
  • Clinical triad of steatorrhea, diabetes and pancreatic calcification
Key pathological features
  • Diffuse fibrosis
  • Loss of acini and ductal tissue
  • Relatively normal islets at early stage
  • Intraductal calculi may present
Hereditary pancreatitis
  • Recurrent severe acute pancreatitis
  • Beginning in childhood and ultimately leading to chronic pancreatitis
  • Abnormally increases or sustains the activity of trypsin
  • Most common: Gain-of-function mutations of trypsinogen (PRSS1)
  • Higher risk of pancreatic cancer
Treatment
  • Pancreatic duct drainage, Whipple resection (relieves pain in 50% of patients with pain)



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