Abstract
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
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