Chronic pancreatitis is a chronic inflammatory process leading to the irreversible destruction and fibrotic replacement of the normal pancreatic tissue.

Parenchyma destruction with fibrotic replacement causes pancreatic loss of function, and this results in exocrine insufficiency (reduced production of pancreatic enzymes with malabsorption, bloating, weight loss and steatorrhea), and in diabetes mellitus (reduced insulin production with persistent hyperglycemia).

Abdominal pain is the dominant clinical problem in patients with chronic pancreatitis. It is commonly described as persistent, deep, penetrating, and localized in the epigastrium, often with radiation to the back. The pathogenesis of pain is multifactorial. Both ductal hypertension (due to chronic obstruction) and neuropathic mechanisms have been proposed to contribute to the pain genesis. Pain in chronic pancreatitis may be particularly hard to treat, and carries a potential for nercotic analgesics addiction. Furthermore, chronic pain impairs appetite and limits food intake, contributing to weight loss and malnutrition. The natural history of pain may be variable: some patients experience acute episodes, in others the pain is chronic since its onset. 

In Western countries, 70-90% of all cases of chronic pancreatitis are related to alcohol abuse. However, only 5-15% of heavy drinkers develop chronic pancreatitis, suggesting important cofactors, for example a diet high in fat and proteins, deficiency in antioxidants, and cigarette smoking. Smoking seems to be an independent etiologic factor, particularly for the formation of calcifications. 

Other less common causes of chronic pancreatitis include:

• Obstruction of the pancreatic duct (stones, benign slow-growing neoplasms)
• Cystic fibrosis
• Pancreas divisum
• Duodenal cystic dystrophy (groove pancreatitis),
• Autoimmune diseases
• Drugs
• Unknown causes

The diagnosis of chronic pancreatitis is based on symptoms (alcohol intake/smoking history, pain, signs of exocrine and/or endocrine insufficiency), laboratory testing (blood glycemia, insulin, oral glucose tolerance test, fecal elastase-1 measurement), genetic testings (CFTR, SPINK-1), and cross-sectional imaging (CT-scan, secretin-enhanced magnetic resonance).

Whereas almost all patients with chronic pancreatitis have an exocrine insufficiency to some degree at the time of diagnosis, this in not the case for endocrine insufficiency. When develops, endocrine insufficiency is similar to type-1 diabetes mellitus, resulting from inflammatory disruption of Langerhans islets. However, the concomitant disruption of glucagon-producing cells (counteracting the insulin function) makes the diabetes associated with chronic pancreatitis particularly hard to control. 

The treatment of chronic pancreatitis is primarily the field of gastroenterologists, with the severe abdominal pain and maldigestion as the domains of conservative measures. The initial approach to patients with maldigeston is to restrict fat intake enough to abolish steatorrhea. Nutrient deficiency is compensated by oral vitamin supplements. When funcional reserve of the pancreas is no longer able to digest fat, pancreatic enzyme replacement therapy is given. Lifestyle is the other mainstay of the management of this patients (discountinuation of alcohol abuse and/or smoking).

As many as 50% of patients with chronic pancreatitis will ultimately require surgical treatments, because conservative medical treatment cannot halt the progression of pain and exocrine and endocrine insufficiency, or pancreatitis-associated complications. These include jaundice and duodenal obstruction, typical of cystic dystrophy of the duodenal wall (known as groove pancreatitis). Furthermore, surgery may be necessary in the suspicion of an underlying malignancy. Cystic dystrophy of the duodenal wall mandates pancreaticoduodenectomy, while “classic” chronic pancreatitis is better treated with derivation procedures. To learn more click here.