PURPOSE OF REVIEW:This paper updates the treatment of Stevens-Johnson syndrome and toxic epidermal necrolysis supported by relevant views about the pathogenesis. RECENT FINDINGS:Building on the thesis that Stevens-Johnson syndrome and toxic epidermal necrolysis are due to dermal cell apoptosis, molecular pathways that may lead to this have been proposed. Intravenous immunoglobulin is postulated to block apoptosis via the Fas pathway. Most series on the use of intravenous immunoglobulin in toxic epidermal necrolysis have been favourable. Tumour necrosis factor is also thought to be an important mediator of cell death in toxic epidermal necrolysis. There was impressive control of the progression of toxic epidermal necrolysis with intravenous anti-tumour necrosis factor antibody infliximab in two cases. Strong associations between human leukocyte antigen subtypes and severe cutaneous reactions due to allopurinol and carbamazepine have been described. SUMMARY:To date, there is no established treatment of Stevens-Johnson syndrome/toxic epidermal necrolysis. With advancing knowledge of the pathogenesis, it is hoped that better forms of treatment may result.

译文

审查目的:本文更新了史蒂文斯-约翰逊综合征和中毒性表皮坏死溶解的治疗方法,并提供了有关发病机理的相关观点。
最近的发现:在史蒂文斯-约翰逊综合征和中毒性表皮坏死溶解是由于真皮细胞凋亡所致的论点的基础上,已经提出了可能导致这种情况的分子途径。假定静脉内免疫球蛋白可通过Fas途径阻断细胞凋亡。关于在有毒的表皮坏死溶解中使用静脉注射免疫球蛋白的大多数系列都是有利的。肿瘤坏死因子也被认为是毒性表皮坏死溶解过程中细胞死亡的重要介质。静脉注射抗肿瘤坏死因子抗体英夫利昔单抗对毒性表皮坏死溶解的进展有令人印象深刻的控制,其中有2例。已经描述了人白细胞抗原亚型与别嘌呤醇和卡马西平引起的严重皮肤反应之间的强关联。
摘要:迄今为止,尚无史蒂文斯-约翰逊综合征/毒性表皮坏死溶解的既定治疗方法。随着对发病机理的深入了解,希望可以产生更好的治疗形式。

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