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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Slow acetylator genotypes as a possible risk factor for infectious mononucleosis-like syndrome induced by salazosulfapyridine.

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.[1]

References

  1. Slow acetylator genotypes as a possible risk factor for infectious mononucleosis-like syndrome induced by salazosulfapyridine. Ohtani, T., Hiroi, A., Sakurane, M., Furukawa, F. Br. J. Dermatol. (2003) [Pubmed]
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