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J Am Acad Dermatol. 2013 Aug;69(2):173.e1-13; quiz 185-6. doi: 10.1016/j.jaad.2013.05.003.

Toxic epidermal necrolysis: Part I. Introduction, history, classification, clinical features, systemic manifestations, etiology, and immunopathogenesis.

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Dermatology, Preventive Medicine, and Pathology, Rutgers University New Jersey Medical School, Newark, New Jersey 07103-2714, USA.


Toxic epidermal necrolysis is a life-threatening, typically drug-induced mucocutaneous disease. It is clinically characterized as a widespread sloughing of the skin and mucosa, including both external and internal surfaces. Histologically, the denuded areas show full thickness epidermal necrosis. The pathogenic mechanism involves antigenic moiety/metabolite, peptide-induced T cell activation, leading to keratinocyte apoptosis through soluble Fas ligand, perforin/granzyme B, tumor necrosis factor-alfa, and nitric oxide. Recent studies have implicated granulysin in toxic epidermal necrolysis apoptosis and have suggested that it may be the pivotal mediator of keratinocyte death.


ALDEN; APC; BSA; CD40 ligand; CD40L; EM; Fas ligand; FasL; HLA; MHC; NF-κB; NK; NO; PBMC; SJS; Stevens–Johnson syndrome; TEN; algorithm for drug causality for epidermal necrolysis; antigen presenting cell; apoptosis; body surface area; drug eruption; erythema multiforme; granulysin; human leukocyte antigen; major histocompatibility complex; natural killer; nitric oxide; nuclear factor kappaB; peripheral blood mononuclear cell; sFasL; serum Fas ligand; toxic epidermal necrolysis

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