Toxic epidermal necrolysis: Review of pathogenesis and management

被引：110

作者：

Downey, Andrew ^{[1
]}

Jackson, Chris ^{[2
]}

Harun, Nadia ^{[3
]}

Cooper, Alan ^{[4
]}

机构：

[1] Univ Sydney, Sydney, NSW 2006, Australia

[2] Kolling Inst Med Res, Sydney, NSW, Australia

[3] Westmead Millennium Inst, Sydney, NSW, Australia

[4] Royal N Shore Hosp, St Leonards, NSW 2065, Australia

来源：

JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY | 2012年 / 66卷 / 06期

关键词：

STEVENS-JOHNSON-SYNDROME; SOLUBLE FAS LIGAND; DOSE INTRAVENOUS IMMUNOGLOBULIN; NECROSIS-FACTOR-ALPHA; T-CELLS; HLA-B-ASTERISK-1502; ALLELE; CUTANEOUS REACTIONS; PLASMA-EXCHANGE; GENE-EXPRESSION; NITRIC-OXIDE;

D O I：

10.1016/j.jaad.2011.09.029

中图分类号：

R75 [皮肤病学与性病学];

学科分类号：

100206 ;

摘要：

Toxic epidermal necrolysis (TEN) is a severe cutaneous drug reaction with a mortality rate of approximately 30%. The hallmark of TEN is widespread epidermal sloughing due to keratinocyte apoptosis. Multiple genetic associations between TEN and specific ethnic populations have been determined. The pathophysiology of TEN has yet to be fully elucidated; however, current pathogenic models implicate Fas ligand, granulysin, and reactive oxygen species. The value of current therapies, such as intravenous immunoglobulin and corticosteroids, remains under evaluation. (J Am Acad Dermatol 2012;66:995-1003.)

引用

页码：995 / 1003

页数：9

共 84 条

[1] Toxic epidermal necrolysis and Stevens-Johnson syndrome are induced by soluble Fas ligand [J].