Association between the N-acetylation genetic polymorphism and aspirin-induced urticartia

N-acetylation represents one of the key pharmacogenetic traits in metabolism of xenobiotics, including drugs. Dominance of ‘slow-acetylators’ has been demonstrated in atopic patients, contact allergy and has been investigated in patients with sulfonamide hypersensitivity. The aim of this survey was to assess genotype of N-acetyltransferase2 (NAT2) polymorphism in patients with aspirin-induced urticaria (AIU). To the study we included 24 consecutive patients with medical history of urticaria induced by aspirin and 123 healthy controls. In the patients’ group oral provocation tests (OPT) up to 565mg cumulative dose of acetylsalicylic acid were performed. The NAT2 alleles (*4-wilde type, *5, *6 and *7) were determined by polymerase chain reaction-restriction fragment length polymorphism method with DNA extracted from peripherial blood. It was observed 53.7% of slow acetylators in the control group, and respectively 66.7%, 83.3% and 100% in the patients with AIU, in patients with positive OPT and in patients with positive reaction in OPT assessed as severe. Statistical significance association between NAT2*5/NAT2*6 genotype and aspirin-induced urticaria was revealed. The linkage of AIU and slow acetylation (NAT2*5/NAT2*6) seems to be highly probable in the patients with medical history of skin hypersensitivity to aspirin confirmed by positive oral provocation test.