Lack of association between arylamine N-acetyltransferase 2 (NAT2) polymorphism and systemic lupus erythematosus.

Abstract

The slow arylamine -acetyltransferase 2 (NAT2) phenotype frequently has been assumed to be associated with an elevated risk to develop a lupus-like syndrome after administration of drugs such as procainamide or hydralazine. Moreover, there are conflicting data on the role of acetylator phenotype as a susceptibility factor for systemic lupus erythematosus (SLE). Because most investigations have previously been conducted with relatively small sample sizes, the present study was performed to clarify the possible association between genotypes and SLE among a large European cohort. In a case-control study, 209 patients with SLE (194 women, 15 men) were enrolled and matched by gender to 209 controls without clinical signs of inflammatory diseases. All SLE patients fulfilled at least four of the revised American College of Rheumatology classification criteria of SLE. was genotyped for seven known mutations by polymerase chain reaction/restriction fragment length polymorphism. The frequency of slow acetylation genotypes in SLE patients (59.8%) did not differ significantly from controls (56.5%). The adjusted odds ratio (OR) was 0.95 (95% confidence interval, 0.59-1.53). Further differentiation to gender, cigarette consumption, allergic disorders and specific SLE manifestations revealed an equal distribution of genotypes in all subgroups. We conclude that this large genotyping study in a Caucasian population demonstrated a lack of evidence for an association of the slow acetylator genotype with SLE.