N-ACETYLTRANSFERASE-2 POLYMORPHISM IN PATIENTS INFECTED WITH HUMAN-IMMUNODEFICIENCY-VIRUS

Objectives: To evaluate the prevalence of slow acetylation of hepatic N-acetyltransferase 2 (NAT2) in patients with different stages of huma n immunodeficiency virus (HIV)infection, to assess the relationship be tween acetylation capacity and the degree of immunosuppression, and to study the concordance between NAT2 phenotype and genotype. Methods: T his prospective study in a consecutive sample of HIV-infected patients was performed in the outpatient department of a university hospital t hat provides primary and tertiary care. The NAT2 genotype was assessed by polymerase chain reaction and restriction fragment length polymorp hism, the NAT2 phenotype was determined by caffeine test (urinary meta bolic ratio of the caffeine metabolites 5-acetylamino-6-formylamino-3- methyluracil and 1-methylxanthine). Results: Fifty patients with Cente rs for Disease Control HIV infection stages A (10 patients), B (20 pat ients), and C (20 patients) were included in the study after each gave informed consent. According to genotyping and phenotyping, 32 (64%) p atients were slow acetylators, with a concordance of the two methods o f 96%. The overall distribution was similar to distributions reported in other white populations. The slow acetylator phenotype was found in seven, 16, and nine patients with stage A, B, and C, respectively. Ei ght of the 10 patients with previous adverse reactions to sulfonamides had slow acetylator phenotypes. Acetylation capacity was independent of CD4 cell counts. Conclusions: This study revealed an excellent agre ement between genotypes and phenotypes of NAT2 in patients with HIV in fection. There was no increase in prevalence of slow acetylation in pa tients with advanced stages of the disease. This apparent discrepancy to an earlier study may be the result of differences in co-medication of the patients studied and may point to the relevance of drug interac tions in the treatment of patients with HIV infection.