重症药疹的基因机制

发布时间：2018-04-29 13:44

本文选题：药物不良反应 + 人类白细胞抗原基因等位基因　；参考：《中国医学文摘(皮肤科学)》2016年06期

【摘要】：重症药疹(SDRs)包括Stevens-Johnson综合征(SJS)、中毒性表皮坏死松解症(TEN)、药物反应伴嗜酸性粒细胞增多和系统症状(DRESS)以及急性泛发性发疹性脓疱病(AGEP)。一旦罹患,不仅影响患者原发疾病的临床治疗,而且因其死亡率高、后遗症多,给患者及社会带来巨大损失。重症药疹的基因研究近年来有重大突破:特定的人类白细胞抗原(HLA)基因目前已被证实与阿巴卡韦、卡马西平、别嘌呤醇、柳氮磺胺吡啶等临床常见药物所致药疹相关;药物/药物代谢产物-HLA分子-T细胞受体(TCR)复合物的形成与重症药疹的发病密切相关;非HLA基因如药物代谢相关酶基因、功能性细胞因子基因多态性亦被发现参与药疹发病。这些研究一方面为药疹发病机制的阐明提供了新的线索;另一方面,进行临床用药前易感HLA等位基因的筛查能很大程度上保证用药的安全性。
[Abstract]:Severe drug rash (SDRs) includes Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (Ten), drug response with eosinophil proliferation and systemic symptoms (DRESS) and acute generalized rash pustulosis (AGEP). Once attacked, it not only affects the clinical treatment of patients with primary diseases, but also brings great losses to patients and society because of its high mortality and more sequelae. In recent years, the gene research of severe drug eruption has made a great breakthrough: the specific HLA-HLA gene has been confirmed to be related to drug rash caused by common clinical drugs such as abacavir, carbamazepine, allopurinol, salbutamepyridine and so on. The formation of drug / drug metabolite HLA molecular T cell receptor complex is closely related to the pathogenesis of severe drug rash, and the polymorphism of non-drug metabolism-related enzyme gene and functional cytokine gene is also found to be involved in the pathogenesis of drug rash. On the one hand, these studies provide new clues to elucidate the pathogenesis of drug eruption; on the other hand, screening susceptible HLA alleles before drug use can largely ensure the safety of drug use.
【作者单位】：复旦大学附属华山医院皮肤科;
【分类号】：R758.25

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