Satapathy Sanjaya K, Kuwajima Vanessa, Nadelson Jeffrey, Atiq Omair, Sanyal Arun J
Methodist University Hospital Transplant Institute, Division of Surgery, University of Tennessee Health Sciences Center, Memphis, Tennessee, USA.
Division of Gastroenterology and Hepatology, University of Tennessee Health Sciences Center, Memphis, Tennessee, USA.
Ann Hepatol. 2015 Nov-Dec;14(6):789-806. doi: 10.5604/16652681.1171749.
Over the past decades, many drugs have been identified, that can potentially induce steatohepatitis in the predisposed individual. Classically this has been incriminated to amiodarone, perhexiline, and 4,4'-diethylaminoethoxyhexestrol (DH), all of which have been found to independently induce the histologic picture of non-alcoholic steatohepatitis (NASH). Pathogenetic mechanisms of hepatotoxicity although still evolving, demonstrate that mitochondrial dysfunction, deranged ATP production and fatty acid catabolism likely play an important role. Drugs like steroid hormones can exacerbate the pathogenetic mechanisms that lead to NASH, and other drugs like tamoxifen, cisplatin and irenotecan have been shown to precipitate latent fatty liver as well. Further research aiming to elucidate the pathogenesis of drug-induced steatosis and steatohepatitis is needed in order to better design therapeutic targets.
在过去几十年中，已确定许多药物可在易感个体中潜在地诱发脂肪性肝炎。传统上，这归咎于胺碘酮、哌克昔林和4,4'-二乙氨基乙氧基己烯雌酚（DH），所有这些药物均已被发现可独立诱发非酒精性脂肪性肝炎（NASH）的组织学表现。肝毒性的发病机制虽仍在演变，但表明线粒体功能障碍、ATP生成紊乱和脂肪酸分解代谢可能起重要作用。类固醇激素等药物可加剧导致NASH的发病机制，而他莫昔芬、顺铂和伊立替康等其他药物也已被证明可促使潜伏性脂肪肝发作。为了更好地设计治疗靶点，需要进一步开展研究以阐明药物性脂肪变性和脂肪性肝炎的发病机制。
