Abstracts: Abstracts of Papers Submitted to the 39th Annual Meeting of the American Pancreatic Association, November 7-8, 2008, Chicago, Illinois
Unlike gallstones, acute intake of alcohol is believed not to be a cause of acute pancreatitis. Based on the current accepted mechanism in which alcohol causes acute pancreatitis, chronic intake daily of over 50 grams per day over many years is expected to cause chronic damage, protein plugs, fibrosis, and/or ductal changes prior to any attack of acute pancreatitis. While many patients with acute pancreatitis attributed to alcohol have evidence of chronic pancreatitis at admission, such as exocrine insufficiency, ductal changes in the pancreas and/or calcifications, the diagnosis is often made in patients with no evidence of chronic disease. In these patients, with alcoholic acute pancreatitis, the diagnosis is made based on the absence of gallstones, a normal triglyceride level and a strong history of alcohol intake despite an otherwise normal appearing pancreas.
In order to better establish whether patients with acute pancreatitis attributed to alcohol, in the absence of imaging evidence of chronic disease, are indeed due to alcohol, we performed the following study. A consecutive series of patients seen in 1998 for acute pancreatitis were studied.
During the study period, 165 patients were admitted with acute pancreatitis. Of these, 58 were diagnosed as having alcohol as the etiology. 38/58 patients were found to have no evidence of chronic pancreatic disease on imaging, CT and/or MRI. Nine of these 38 patients were identified on follow-up, mean 9.6 years. Of these nine patients with acute pancreatitis attributed to alcohol based on history almost 10 years prior, 7/9 had no further episodes of acute pancreatitis. 5/9 patients described themselves as abstinent from alcohol use. 4/5 continued using alcohol in moderation 3/5, or heavily 1/5. Imaging had been performed within the past year in 6/9. There was no evidence of chronic pancreatitis in any of these patients defined by ductal abnormalities and/or calcifications. 3/9 of these patients had evidence of gallstones on imaging. None of the patients had any evidence of pancreatic exocrine insufficiency.
Although there was limited follow-up, this study suggests that many patients, perhaps most patients with alcoholic acute pancreatitis may have another etiology such as gallstones. Despite a history of alcohol consumption, it remains unclear whether alcohol causes acute pancreatitis in the absence of evidence of chronic pancreatic disease at admission.