Clinical meaning
Chronic pancreatitis involves progressive inflammatory destruction of pancreatic parenchyma with replacement by fibrotic tissue, leading to irreversible loss of exocrine (digestive enzymes) and endocrine (insulin, glucagon) function. Alcohol is the most common cause (60–70%), followed by genetic mutations (PRSS1, CFTR, SPINK1), autoimmune pancreatitis, and idiopathic causes. The sentinel acute pancreatitis event (SAPE) hypothesis proposes that an initial acute episode activates pancreatic stellate cells, which produce collagen and drive fibrosis through repeated injury-repair cycles. Progressive fibrosis causes ductal obstruction, calcification, and nerve damage producing chronic severe pain.
Diagnosis & workup
Diagnostics & workup: - CT abdomen showing pancreatic calcifications (pathognomonic), ductal dilation, parenchymal atrophy - MRCP for ductal anatomy (dilation, strictures, stones) - Endoscopic ultrasound (EUS)—most sensitive for early chronic pancreatitis - Fecal elastase-1 < 200 μg/g confirms exocrine insufficiency - 72-hour fecal fat collection for steatorrhea quantification - HbA1C and fasting glucose for endocrine insufficiency (type 3c diabetes) - IgG4 levels if autoimmune pancreatitis suspected