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Vol. 20, No. 2, 2007
Issue release date: March 2007
Section title: Original Paper
Skin Pharmacol Appl Skin Physiol 2007;20:66–70
(DOI:10.1159/000097652)

Glutathione-S-Transferase Pi Expression in Toxic Epidermal Necrolysis: A Marker of Putative Oxidative Stress in Keratinocytes

Paquet P. · Piérard G.E.
Department of Dermatopathology, University of Liège, Liège, Belgium

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 3/31/2006
Accepted: 7/6/2006
Published online: 12/1/2006
Issue release date: March 2007

Number of Print Pages: 5
Number of Figures: 1
Number of Tables: 2

ISSN: 1660-5527 (Print)
eISSN: 1660-5535 (Online)

For additional information: http://www.karger.com/SPP

Abstract

Background: Toxic epidermal necrolysis (TEN) is a dramatic drug-induced emergency related to extensive destruction of the epidermis. There is evidence that its pathomechanism involves impaired detoxication of xenobiotics. Glutathione-S-transferase π (GST-π) is a phase II detoxifying enzyme involved in drug metabolization by human keratinocytes. Method: Immunohistochemistry was performed in order to assess the expression of GST-π in keratinocytes of TEN, other cutaneous adverse drug reactions and bullous pemphigoid. Results: GST-π was disclosed in the involved epidermis of 16/16 TEN patients. It was present in the cytoplasm of suprabasal keratinocytes. GST-π was also expressed in the clinically uninvolved skin in a majority (8/12) of TEN patients. By contrast, it was rarely and poorly expressed in the other tested dermatoses. Conclusion: The pathomechanism of TEN is not related to an impaired quantitative expression of GST-π. GST-π expression is an early event in TEN. As oxidative stress is a major inducer of GST-π, this mechanism might be involved in TEN. Its GST-π expression mainly restricted to the suprabasal keratinocytes suggests that the pathomechanisms leading to keratinocyte death in TEN are distinct at different levels of the epidermis.

© 2007 S. Karger AG, Basel


  

Author Contacts

Dr. P. Paquet
Department of Dermatopathology
CHU Sart-Tilman
BE–4000 Liège (Belgium)
Tel. +32 4 366 2408, Fax +32 4 366 2976, E-Mail P.Paquet@chu.ulg.ac.be

  

Article Information

Received: March 31, 2006
Accepted: July 6, 2006
Published online: December 1, 2006
Number of Print Pages : 5
Number of Figures : 1, Number of Tables : 2, Number of References : 25

  

Publication Details

Skin Pharmacology and Physiology (Journal of Pharmacological and Biophysical Research)

Vol. 20, No. 2, Year 2007 (Cover Date: March 2007)

Journal Editor: Lademann, J. (Berlin)
ISSN: 1660–5527 (print), 1660–5535 (Online)

For additional information: http://www.karger.com/SPP


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 3/31/2006
Accepted: 7/6/2006
Published online: 12/1/2006
Issue release date: March 2007

Number of Print Pages: 5
Number of Figures: 1
Number of Tables: 2

ISSN: 1660-5527 (Print)
eISSN: 1660-5535 (Online)

For additional information: http://www.karger.com/SPP


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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in goverment regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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