Apte M V, Haber P S, Norton I D, Wilson J S
Pancreatic Research Group, Department of Gastroenterology, Prince of Wales Hospital and University of New South Wales, Sydney, Australia.
Addict Biol. 1998 Apr;3(2):137-50. doi: 10.1080/13556219872209.
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.
酒精性胰腺炎是酒精滥用的一种主要且常致命的并发症。直到最近，人们普遍认为酒精性胰腺炎从一开始就是一种慢性疾病。然而，现在有新出现的证据支持坏死-纤维化假说，即酒精性胰腺炎始于急性过程，反复的急性发作导致慢性胰腺炎，进而导致外分泌和内分泌功能衰竭。在过去10至15年中，酒精性胰腺炎发病机制的研究重点已从可能的括约肌和导管异常转向腺泡细胞本身，越来越多的证据表明腺泡细胞是初始损伤部位。最近的研究表明，腺泡细胞代谢酒精的速度与肝细胞中观察到的速度相当。此外，已经证明酒精及其代谢产物对胰腺腺泡细胞有直接影响，可能促进消化酶过早激活和氧化应激。确定该疾病的易感因素和触发因素仍然是一项挑战。
