Dreiling and Koller (31) have reported that, given 100 alcoholics, 5 will develop clinical acute pancreatitis, 15 will develop alcoholic cirrhosis, while only 1 will develop clinical evidence of both diseases. If, after the first attack of pancreatitis, patients continue to drink at the same level as that prior to the first attack of pancreatitis, their risk of repeated acute attacks leading to chronic pancreatic injury is reported to be around 41%, while with reduced drinking the risk falls to 23% and with abstinence or with occasional alcohol intake, decreases further to 14% (98).Īlthough the increased risk of pancreatitis with alcohol abuse is unquestioned, it is well acknowledged that the overall frequency of the disease (at least in terms of overt clinical illness) is low, with clinically evident acute pancreatitis seen in only up to 3-5% of heavy drinkers (55, 59, 116). A meta-analysis of several relevant studies has calculated the threshold to be 4 drinks/day for chronic pancreatitis (54). A population based cohort study has reported that alcohol increases the risk of pancreatitis in a dose dependent manner (55), while a large case-control study has proposed a threshold of 5 drinks per day as the baseline for the risk of developing alcoholic chronic pancreatitis (117). Epidemiology of alcoholic pancreatitisĪlcohol abuse is ranked as the second most common cause of acute pancreatitis (after gallstone disease) (119), but is well established as the single most common cause of chronic pancreatitis, with an attributable risk of 40% (25, 43). This implies that additional factors may confer susceptibility to alcoholic pancreatitis in some drinkers.Ģ. maldigestion, and in advanced cases, diabetes.ĭespite, the well-established association of alcohol abuse and pancreatitis, there is an acknowledged clinical paradox in the field– on the one hand, the risk of developing the disease increases with increasing consumption of alcohol (55) - but on the other, only a minority of heavy drinkers (<5%) develop clinically evident pancreatic disease (32, 117). Repeated attacks of necroinflammation can then lead to chronic changes in the pancreas including acinar atrophy and fibrosis (chronic pancreatitis), with patients suffering from chronic pain, symptoms of pancreatic insufficiency i.e. An acute episode of pancreatic necroinflammation (acute pancreatitis) is characterised by acute abdominal pain and raised serum amylase and lipase levels. This was subsequently confirmed by Freidrich (41) in 1878 and Fitz (35) in 1889, using a more detailed analytical approach.Īlcoholic pancreatitis is now generally recognised to have both acute and chronic manifestations. Alcoholic pancreatitis is now increasingly thought to be a multifactorial condition, where, in addition to alcohol, other lifestyle and inherited agents may determine the initiation and course of the disease.ĭamage to the pancreas as a result of alcohol * abuse was first recognised as early as two hundred years ago, with reports published in 1815 describing an association between heavy drinking and the development of pancreatitis (22, 37). In terms of lifestyle factors, smoking is emerging as an important factor in the development/progression of alcoholic pancreatitis. Polymorphisms/mutations of genes encoding alcohol metabolising enzymes, digestive enzymes and their inhibitors and the tight junction protein claudin-2 have been described in alcoholics with pancreatitis. With regard to individual susceptibility factors that may cause overt pancreatitis in some drinkers, both inherited and lifestyle factors have been studied. The three major cell types in the pancreas affected by alcohol exposure include acinar cells, ductal cells and stellate cells damage to these cells drives the acinar cell death, calcification and fibrosis of alcoholic pancreatitis. Recent experimental evidence indicates that endotoxinemia (known to occur in alcoholics secondary to an alcohol-induced increase in gut mucosal permeability), may be an important co-factor in alcohol-related pancreatic injury. Evidence from in vivo and in vitro studies indicates that the detrimental effects of alcohol on the pancreas are most likely due to direct toxic effects of its metabolites (such as acetaldehyde and fatty acid ethyl esters), and/or the by-products of ethanol metabolism such as reactive oxygen species. However, not all heavy drinkers develop clinical pancreatitis, suggesting that additional trigger factor(s) may be required to initiate overt disease. The risk of developing pancreatitis increases with increased consumption of alcohol. Alcohol abuse is a well-recognised association of both acute and chronic pancreatitis, with repeated attacks of alcohol-induced acute pancreatic necroinflammation leading to chronic disease.
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