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Alcoholic liver disease

机译：酒精性肝病

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Research has substantiated the role of several mechanisms responsible for alcohol-induced hepatotoxicity. These mechanisms include: oxidative stress and lipid peroxidation; immuno-genic processes initiated by formation of protein adducts of acetaldehyde, other aldehydes and 1 -hydroxyethyl radicals; and activation of Kupffer cells by endotoxin and subsequent cascade of events that involved cytokines, chemokines, and adhesion molecules. Increasing evidence implicates enhanced intestinal permeability caused by alcohol ingestion as the culprit that leads to endotoxemia. While oxidative stress is important, the principal source of reactive oxygen species that causes alcohol-induced liver injury is hotly debated. Potential sources may include cytochrome P450IIE1, activated Kupffer cells, and mitochondrial electron transfer chain. Apoptosis is likely an important pathway that culminates in hepatocyte cell death. Abstinence, corticos-teroids, and enteral nutrition remain the cornerstones in the treatment of alcoholic hepatitis. The efficacies of medications such as S-adenosylmethionine and pentoxifylline will need further confirmation by additional randomized trials before they can be recommended as standard therapies for alcoholic hepatitis.
机译：研究证实了几种机制可导致酒精引起的肝毒性。这些机制包括：氧化应激和脂质过氧化;通过形成乙醛，其他醛和1-羟乙基自由基的蛋白质加合物而引发的免疫原性过程;内毒素对库普弗细胞的激活和随后的一系列涉及细胞因子，趋化因子和粘附分子的事件的激活。越来越多的证据表明，酒精摄入是导致内毒素血症的罪魁祸首，肠道通透性增强。尽管氧化应激很重要，但引起酒精引起的肝损伤的活性氧的主要来源却引起了激烈的争论。潜在来源可能包括细胞色素P450IIE1，活化的Kupffer细胞和线粒体电子转移链。凋亡可能是导致肝细胞死亡的重要途径。禁欲，皮质类固醇和肠内营养仍然是治疗酒精性肝炎的基石。 S-腺苷甲硫氨酸和己酮可可碱等药物的疗效需要通过其他随机试验进一步证实，然后才能推荐作为酒精性肝炎的标准疗法。

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