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史蒂文斯-约翰逊综合征和中毒性表皮坏死松解症的最新观点。

Current Perspectives on Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis.

机构信息

Allergy/Dermatology Unit, Department of Internal Medicine, Kantonsspital Winterthur, Winterthur, Switzerland.

Department of Dermatology, Bellinzona Regional Hospital, Bellinzona, Switzerland.

出版信息

Clin Rev Allergy Immunol. 2018 Feb;54(1):147-176. doi: 10.1007/s12016-017-8654-z.

Abstract

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are considered a delayed-type hypersensitivity reaction to drugs. They represent true medical emergencies and an early recognition and appropriate management is decisive for the survival. SJS/TEN manifest with an "influenza-like" prodromal phase (malaise, fever), followed by painful cutaneous and mucous membrane (ocular, oral, and genital) lesions, and other systemic symptoms. The difference between SJS, SJS/TEN overlap, and TEN is defined by the degree of skin detachment: SJS is defined as skin involvement of < 10%, TEN is defined as skin involvement of > 30%, and SJS/TEN overlap as 10-30% skin involvement. The diagnosis of different degrees of epidermal necrolysis is based on the clinical assessment in conjunction with the corresponding histopathology. The mortality rates for SJS and TEN have decreased in the last decades. Today, the severity-of-illness score for toxic epidermal necrolysis (SCORTEN) is available for SJS/TEN severity assessment. Drugs with a high risk of causing SJS/TEN are anti-infective sulfonamides, anti-epileptic drugs, non-steroidal anti-inflammatory drugs of the oxicam type, allopurinol, nevirapine, and chlormezanone. Besides conventional drugs, herbal remedies and new biologicals should be considered as causative agents. The increased risk of hypersensitivity reactions to certain drugs may be linked to specific HLA antigens. Our understanding of the pathogenesis of SJS/TEN has improved: drug-specific T cell-mediated cytotoxicity, genetic linkage with HLA- and non-HLA-genes, TCR restriction, and cytotoxicity mechanisms were clarified. However, many factors contributing to epidermal necrolysis still have to be identified, especially in virus-induced and autoimmune forms of epidermal necrolysis not related to drugs. In SJS/TEN, the most common complications are ocular, cutaneous, or renal. Nasopharyngeal, esophageal, and genital mucosal involvement with blisters, erosions as well as secondary development of strictures also play a role. However, in the acute phase, septicemia is a leading cause of morbidity and fatality. Pulmonary and hepatic involvement is frequent. The acute management of SJS/TEN requires a multidisciplinary approach. Immediate withdrawal of potentially causative drugs is mandatory. Prompt referral to an appropriate medical center for specific supportive treatment is of utmost importance. The most frequently used treatments for SJS/TEN are systemic corticosteroids, immunoglobulins, and cyclosporine A.

摘要

史蒂文斯-约翰逊综合征(SJS)和中毒性表皮坏死松解症(TEN)被认为是一种药物引起的迟发型超敏反应。它们是真正的医疗急症,早期识别和适当的治疗对于生存至关重要。SJS/TEN 表现为“流感样”前驱期(不适、发热),随后出现疼痛性皮肤和黏膜(眼部、口腔和生殖器)损伤和其他全身症状。SJS、SJS/TEN 重叠和 TEN 的区别在于皮肤脱落的程度:SJS 定义为皮肤受累<10%,TEN 定义为皮肤受累>30%,SJS/TEN 重叠为 10-30%皮肤受累。不同程度表皮坏死松解症的诊断基于临床评估结合相应的组织病理学。在过去几十年中,SJS 和 TEN 的死亡率有所下降。如今,已可用于 SJS/TEN 严重程度评估的毒性表皮坏死松解症严重程度评分(SCORTEN)。具有引起 SJS/TEN 高风险的药物为抗感染磺胺类药物、抗癫痫药物、oxicam 类非甾体抗炎药、别嘌呤醇、奈韦拉平、氯米扎酮。除传统药物外,草药和新型生物制剂也应被视为致病因素。某些药物引起的过敏反应风险增加可能与特定 HLA 抗原有关。我们对 SJS/TEN 发病机制的认识有所提高:药物特异性 T 细胞介导的细胞毒性、与 HLA 和非 HLA 基因的遗传联系、TCR 限制和细胞毒性机制已得到阐明。然而,仍有许多导致表皮坏死松解的因素有待确定,尤其是与药物无关的病毒诱导和自身免疫性表皮坏死松解形式。在 SJS/TEN 中,最常见的并发症是眼部、皮肤或肾脏。鼻咽、食管和生殖器黏膜水疱、糜烂以及继发狭窄也很常见。然而,在急性期,败血症是发病率和死亡率的主要原因。肺部和肝脏受累很常见。SJS/TEN 的急性治疗需要多学科方法。必须立即停用可能引起疾病的药物。及时转至适当的医疗中心进行特定的支持性治疗至关重要。SJS/TEN 最常用的治疗方法是全身性皮质类固醇、免疫球蛋白和环孢素 A。

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