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Slow acetylator genotypes as a possible risk factor for infectious mononucleosis‐like syndrome induced by salazosulfapyridine
Author(s) -
Ohtani T.,
Hiroi A.,
Sakurane M.,
Furukawa F.
Publication year - 2003
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1046/j.1365-2133.2003.05321.x
Subject(s) - medicine , dermatology , family medicine
Summary We report two patients with infectious mononucleosis‐like syndrome induced by salazosulfapyridine (SASP). In both cases, high fever, skin rash, liver dysfunction and atypical lymphocytosis developed 3 weeks after initiating treatment with SASP. SASP is known to be mainly metabolized by N ‐acetyltransferase 2 (NAT2), and acetylation phenotypes (rapid, intermediate and slow acetylator) correlate with NAT2 * genotypes. In our two patients, we investigated NAT2 * genotypes by the polymerase chain reaction–restriction fragment length polymorphism method. We identified NAT2 * 6/ * 7 in one patient, and NAT2 * 6/ * 5 in the other, suggesting that both were slow acetylator phenotypes. In 20 healthy volunteers we found no slow acetylator genotypes. Genotyping prior to medication may be useful in evaluating patients with a high risk of severe systemic reaction to SASP.