ALCOHOL AND THE PANCREAS

Alcoholic pancreatitis is a major, often lethal complication of alcoho l abuse. Until recently it was generally accepted that alcoholic pancr eatitis was a chronic disease from the outset. However, there is now e merging evidence in favour of the necrosis-fibrosis hypothesis that al coholic pancreatitis begins as an acute process and that repented acut e attacks lead to chronic pancreatitis, resulting in exocrine and endo crine failure. Over the past 10-15 years, the focus of research into t he pathogenesis of alcoholic pancreatitis has shifted from possible sp hincteric and ductular abnormalities to the acinar cell itself which h as increasingly been implicated as the initial see of injury. Recent s tudies 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 enzy me activation and oxidant stress. The challenge remains to identify pr edisposing and triggering factors in this disease.