Chronic Pancreatitis I: Introduction

Chronic pancreatitis is a long-standing, relapsing inflammation of the pancreas, characterized by irreversible damage to the gland. It results in progressive destruction of the pancreatic parenchyma, fibrosis, and eventual loss of both exocrine and endocrine function. The disease may evolve gradually after multiple episodes of acute pancreatitis or develop independently.

Etiology

Chronic pancreatitis can arise from a variety of causes:

• Alcohol use is the leading cause, accounting for 70–80% of cases. Long-term heavy consumption damages acinar cells and promotes the formation of protein plugs.
• Smoking is an independent, dose-related risk factor. When combined with alcohol use, it significantly increases disease risk.
• Genetic mutations include PRSS1 (cationic trypsinogen), CFTR (cystic fibrosis transmembrane conductance regulator), SPINK1, and others. These mutations can disrupt enzyme regulation or ductal secretion.
• Ductal obstruction from tumors, strictures, cysts, or trauma can lead to local inflammation and fibrosis.
• Hypercalcemia, such as that caused by hyperparathyroidism, can promote intraductal calcium precipitation.
• Autoimmune mechanisms, nutrient deficiencies (as seen in tropical pancreatitis), and idiopathic cases also contribute.

Clinical Features

• Pain: Recurrent or persistent upper abdominal pain, often triggered by meals and possibly radiating to the back.
• Exocrine insufficiency: As enzyme secretion declines, patients may experience steatorrhea, bloating, malabsorption, and weight loss.
• Endocrine insufficiency: Loss of islet cells can lead to insulin-dependent diabetes.
• Complications: Ductal stones, pseudocysts, and an increased risk of pancreatic cancer may happen in advanced stages.