Alcohol and the pancreas

Abstract

Alcoholic pancreatitis is a major, often lethal complication of alcohol abuse. Until recently it was generally accepted that alcoholic pancreatitis was a chronic disease from the outset. However, there is now emerging evidence in favour of the necrosis-fibrosis hypothesis that alcoholic pancreatitis begins as an acute process and that repeated acute attacks lead to chronic pancreatitis, resulting in exocrine and endocrine failure. Over the past 10-15 years, the focus of research into the pathogenesis of alcoholic pancreatitis has shifted from possible sphincteric and ductular abnormalities to the acinar cell itself which has increasingly been implicated as the initial site of injury. Recent studies have shown that the acinar cell can metabolize alcohol at rates comparable to those observed in hepatocytes. In addition, it has been demonstrated that alcohol and its metabolites exert direct effects on the pancreatic acinar cell which may promote premature digestive enzyme activation and oxidant stress. The challenge remains to identify predisposing and triggering factors in this disease.