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Delayed reepithelialization and scarring deregulation following drug-induced toxic epidermal necrolysis.

作者信息

Paquet P, Jacob E, Quatresooz P, Jacquemin D, Piérard G E

机构信息

Department of Dermatopathology, University Hospital Sart Tilman, CHU, Sart Tilman, B-4000, Liège, Belgium.

出版信息

Burns. 2007 Feb;33(1):100-4. doi: 10.1016/j.burns.2006.04.031. Epub 2006 Oct 31.

DOI:10.1016/j.burns.2006.04.031
PMID:17079086
Abstract

A 51-year-old Caucasian woman developed severe drug-induced toxic epidermal necrolysis (TEN) due to allopurinol. The withdrawal of the culprit drug was unfortunately delayed, and dramatic retardation of reepithelialization was observed. At that stage of disease evolution, an inflammatory cell infiltrate was present in the dermis. Coverage of eroded lesions by frozen cultured keratinocyte allografts failed to hasten reepithelialization compared to ungrafted sites. This unusual protracted TEN evolution was followed by the development of extensive hypertrophic and keloid scars. Several biopsies were taken over 6 months. The histologic presentation of the grafted and ungrafted eroded scar tissues looked similar. Both the number and size of the Factor XIIIa-positive dermal dendrocytes, as well as the number of alpha-actin-positive myofibroblasts showed a marked increase between weeks 2 and 12 after grafting. They were reduced after 6 months when the scarring process was stabilized. alpha1 [IV] collagen was never expressed over the eroded scars. Similar to burn patients, delayed reepithelialization might be a risk factor for abnormal scarring in TEN. Cultured keratinocyte allograft apparently offered no improvement in reepithelialization and did not prevent abnormal scarring in this TEN patient.

摘要

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