Anagen Effluvium as an Early Sign of Azathioprine Toxicity.

Q3 Medicine
Sehtaj Kaur, Asit Kumar Mittal, Shaifali Jain, Laxman Kumar
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引用次数: 0

Abstract

Azathioprine is a purine analog which is Food and Drug Administration (FDA) approved for organ transplant and severe rheumatoid arthritis (RA). Off-label use in dermatological diseases like immunobullous diseases, atopic dermatitis, autoimmune connective tissue disorders like systemic lupus erythematosus (SLE) and dermatomyositis, and other medical conditions like Crohn's disease, Churg-Strauss syndrome, and myasthenia gravis has long been in the picture.1-3 The active metabolite of this prodrug is 6-thioguanine (6-TG), which gets incorporated into DNA/RNA structure, causing decreased purine metabolism resulting in its immunosuppressive effect. Thiopurine methyltransferase (TPMT) converts 6-mercaptopurine (6-MP) to an inactive metabolite. TPMT deficiency will cause increased conversion of 6-MP to active metabolite 6-TG, which increases the risk of myelosuppression, one of the life-threatening side effects of the drug.1,2.

氮唑嘌呤毒性的早期征兆:厌氧原排出物。
硫唑嘌呤是一种嘌呤类似物,被美国食品和药物管理局(FDA)批准用于器官移植和严重类风湿关节炎(RA)。在皮肤疾病,如免疫大疱性疾病、特应性皮炎、自身免疫性结缔组织疾病,如系统性红斑狼疮(SLE)和皮肌炎,以及其他医疗条件,如克罗恩病、丘格-施特劳斯综合征和重症肌无力等方面的适应症外用药早已出现。1-3该前药的活性代谢物为6-硫鸟嘌呤(6-TG),其被并入DNA/RNA结构,导致嘌呤代谢减少,从而产生免疫抑制作用。硫嘌呤甲基转移酶(TPMT)将6-巯基嘌呤(6-MP)转化为无活性代谢物。TPMT缺乏会导致6-MP向活性代谢物6-TG的转化增加,从而增加骨髓抑制的风险,这是该药物危及生命的副作用之一。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
0.80
自引率
0.00%
发文量
509
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