A Fresh Look at the Mechanism of Isoniazid-Induced Hepatotoxicity
A Fresh Look at the Mechanism of Isoniazid-Induced Hepatotoxicity
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DOI：
10.1038/clpt.2010.355
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发表时间：
2011-06-01
影响因子：
6.7
通讯作者：
Uetrecht, J. P.
中科院分区：
文献类型：
--
作者：
Metushi, I. G.;Cai, P.;Uetrecht, J. P.
异烟肼（INH）诱导的肝毒性仍然是一个重要的临床问题，目前的机制假设是不完整的;它被简单地称为代谢特异质，1这被认为是涉及由乙酰肼（INH的代谢物）的生物活化引起的细胞毒性。然而，这一假设是基于动物研究，涉及与人类肝毒性相关的特征非常不同的特征，例如延迟发作。因此，这一问题值得重新审视。
Isoniazid (INH)-induced hepatotoxicity remains a significant clinical problem, and the current mechanistic hypothesis is incomplete; it is simply referred to as metabolic idiosyncrasy, 1 which is believed to involve cytotoxicity caused by bioactivation of acetylhydrazine, 2 a metabolite of INH. However, this hypothesis is based on animal studies, involving characteristics that are very different from those that pertain to hepatotoxicity in humans, such as delayed onset. This issue therefore deserves a fresh look.