作者: Alba Rocco , Debora Compare , Debora Angrisani , Marco Sanduzzi Zamparelli , Gerardo Nardone
DOI: 10.3748/WJG.V20.I40.14652
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摘要: The harmful use of alcohol is a worldwide problem. It has been estimated that abuse represents the world's third largest risk factor for disease and disability; it causal 60 types diseases injuries concurrent cause at least 200 others. Liver main organ responsible metabolizing ethanol, thus considered long time major victim alcohol. Ethanol its bioactive products, acetaldehyde-acetate, fatty acid ethanol esters, ethanol-protein adducts, have regarded as hepatotoxins directly indirectly exert their toxic effect on liver. A similar mechanism postulated alcohol-related pancreatic damage. Alcohol metabolites injure acinar cells elicit stellate to produce deposit extracellular matrix triggering "necrosis-fibrosis" sequence finally leads atrophy fibrosis, morphological hallmarks alcoholic chronic pancreatitis. Even if less attention paid upper lower gastrointestinal tract, produces effects by inducing: (1) direct damaging mucosa esophagus stomach; (2) modification sphincterial pressure impairment motility; (3) alteration gastric output. In intestine, can damage intestinal or altering resident microflora impairing mucosal immune system. Notably, disruption barrier small large intestine contribute liver This review summarizes most clinically relevant digestive tract focusing pathogenic mechanisms which damages liver, pancreas tract.