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影响药物性肝损伤的因素:以抗甲状腺药物为例。

Factors affecting drug-induced liver injury: antithyroid drugs as instances.

作者信息

Heidari Reza, Niknahad Hossein, Jamshidzadeh Akram, Abdoli Narges

机构信息

Pharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.

Pharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. ; Pharmacology and Toxicology Department, Faculty of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran.

出版信息

Clin Mol Hepatol. 2014 Sep;20(3):237-48. doi: 10.3350/cmh.2014.20.3.237. Epub 2014 Sep 25.

DOI:10.3350/cmh.2014.20.3.237
PMID:25320726
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4197171/
Abstract

Methimazole and propylthiouracil have been used in the management of hyperthyroidism for more than half a century. However, hepatotoxicity is one of the most deleterious side effects associated with these medications. The mechanism(s) of hepatic injury induced by antithyroid agents is not fully recognized yet. Furthermore, there are no specific tools for predicting the occurrence of hepatotoxicity induced by these drugs. The purpose of this article is to give an overview on possible susceptibility factors in liver injury induced by antithyroid agents. Age, gender, metabolism characteristics, alcohol consumption, underlying diseases, immunologic mechanisms, and drug interactions are involved in enhancing antithyroid drugs-induced hepatic damage. An outline on the clinically used treatments for antithyroid drugs-induced hepatotoxicity and the potential therapeutic strategies found to be effective against this complication are also discussed.

摘要

甲巯咪唑和丙硫氧嘧啶用于治疗甲状腺功能亢进已有半个多世纪。然而,肝毒性是与这些药物相关的最有害的副作用之一。抗甲状腺药物引起肝损伤的机制尚未完全明确。此外,尚无预测这些药物所致肝毒性发生的特异性工具。本文旨在概述抗甲状腺药物所致肝损伤可能的易感性因素。年龄、性别、代谢特征、饮酒、基础疾病、免疫机制和药物相互作用均与抗甲状腺药物所致肝损伤的加重有关。本文还讨论了抗甲状腺药物所致肝毒性的临床常用治疗方法以及已发现的对该并发症有效的潜在治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7950/4197171/8aa0a5933908/cmh-20-237-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7950/4197171/6a970c01afed/cmh-20-237-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7950/4197171/ba77d40d16fc/cmh-20-237-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7950/4197171/daefea0c3461/cmh-20-237-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7950/4197171/5a6fb8740bee/cmh-20-237-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7950/4197171/8aa0a5933908/cmh-20-237-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7950/4197171/6a970c01afed/cmh-20-237-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7950/4197171/ba77d40d16fc/cmh-20-237-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7950/4197171/daefea0c3461/cmh-20-237-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7950/4197171/5a6fb8740bee/cmh-20-237-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7950/4197171/8aa0a5933908/cmh-20-237-g005.jpg

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Effects of Enzyme Induction and/or Glutathione Depletion on Methimazole-Induced Hepatotoxicity in Mice and the Protective Role of N-Acetylcysteine.酶诱导和/或谷胱甘肽耗竭对小鼠甲巯咪唑诱导的肝毒性的影响及N-乙酰半胱氨酸的保护作用。
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