Toxic epidermal necrolysis : Part I. Introduction, history, classification, clinical features, systemic manifestations, etiology, and immunopathogenesis - 17/07/13

Doi : 10.1016/j.jaad.2013.05.003

Robert A. Schwartz, MD, MPH, DSc (Hon), FRCP (Edin) ^⁎ , Patrick H. McDonough, MD, Brian W. Lee, MD, MS
Dermatology, Preventive Medicine, and Pathology, Rutgers University New Jersey Medical School, Newark, New Jersey

^∗Reprint requests: Robert A. Schwartz, MD, MPH, DSc (Hon), FRCP (Edin), Professor & Head, Dermatology, Rutgers University New Jersey Medical School, Medical Sciences Building H-576, 185 S Orange Ave, Newark, NJ 07103-2714.

Abstract

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.

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Key words : apoptosis, drug eruption, erythema multiforme, granulysin, Stevens–Johnson syndrome, toxic epidermal necrolysis

Abbreviations used : ALDEN, APC, BSA, CD40L, EM, FasL, HLA, MHC, NF-κB, NK, NO, PBMC, sFasL, SJS, TEN

Plan

Toxic epidermal necrolysis

History

Classification

Clinical features

Systemic manifestations

Etiology

Immunopathogenesis

Etiology of apoptosis

Conclusion

	Dr McDonough is currently affiliated with Dermatology, University of Texas Southwestern Medical School, Dallas, Texas.
	Funding sources: None.
	Conflicts of interest: None declared.