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  Vol. 130 No. 5, May 1994 TABLE OF CONTENTS
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Drug Rashes

What Are the Targets of Cell-Mediated Cytotoxicity?

Olivier Chosidow, MD; Isabelle Bourgault, MD; Jean-Claude Roujeau, MD

Arch Dermatol. 1994;130(5):627-629.

Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

ADVANCES ON toxic epidermal necrolysis (TEN) and, more generally, on drug rashes have been achieved recently in three directions: ( 1 ) patients infected with human immunodeficiency virus (HIV) and moreover those profundly immunodepressed are at highly increased risk; (2) most patients with severe adverse skin reactions have an abnormal metabolism of the offending drug; and (3) accumulated pieces of evidence suggest that epidermal necrosis results from cell-mediated cytotoxicity.

In our opinion, any hypothesis on the mechanisms of TEN and other drug rashes should include all these recent and apparently paradoxical data.

INCREASED RATES OF DRUG RASHES IN VIRAL INFECTIONS

In 1967, for the first time, a pediatric resident noticed an unexpectedly high frequency of drug rashes to ampicillin during infectious mononucleosis.1 This high rate of skin reactions to ampicillin (80% to 100%) in patients with acute Epstein-Barr virus (EBV) infection was quickly confirmed.2 It was later observed with other . . . [Full Text PDF of this Article]


Author Affiliations

Unité de Dermatologie Service de Médecine Interne Université Paris VI, Hôpital Pitié-Salpêtrière 75013 Paris, France; Créteil, France



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