BACKGROUND AND AIMS: Allergic asthma is a chronic inflammatory disorder of the airways where, on exposure to allergens, the body mounts an immune response. The etiology of asthma is complex and multifactorial. Rapid and slow acetylators reflect the genetically determined variation in the elimination of xenobiotics. Recent advances have demonstrated the importance of genetic and environmental factors in the development of atopic asthma. Hepatic arylamine N-acetyltransferase 2 (NAT2) takes part in the detoxification of some drugs and arylamine xenobiotics. The aim of the present study was to determine the NAT2 polymorphism in patients with atopic asthma. METHODS: In the study, 184 unrelated asthmatic patients and 181 healthy controls were included. The mutations at positions 481T, 803G, 590A and 857A of the NAT2 gene were determined by a polymerase chain reaction-restriction fragment length polymorphism assay (PCR-RFLP). RESULTS: The frequency of homozygous fast acetylators did not differ significantly between patients and controls. Compared with the control population, the significant prevalence of slow acetylators in the group of patients with atopic asthma was observed. There was a statistically significant prevalence of subjects with NAT2*5/NAT2*5 and NAT2*5/NAT2*6 genotypes. The risk of an atopic asthma development was 3.4 times greater in slow than in fast acetylators (OR = 3.3657; p <0.000001, 95% CI = 2.1282-5.3228). CONCLUSIONS: These results suggest that NAT2 polymorphism may be involved in the pathogenesis of atopic asthma.
BACKGROUND AND AIMS: Allergic asthma is a chronic inflammatory disorder of the airways where, on exposure to allergens, the body mounts an immune response. The etiology of asthma is complex and multifactorial. Rapid and slow acetylators reflect the genetically determined variation in the elimination of xenobiotics. Recent advances have demonstrated the importance of genetic and environmental factors in the development of atopic asthma. Hepatic arylamine N-acetyltransferase 2 (NAT2) takes part in the detoxification of some drugs and arylamine xenobiotics. The aim of the present study was to determine the NAT2 polymorphism in patients with atopic asthma. METHODS: In the study, 184 unrelated asthmatic patients and 181 healthy controls were included. The mutations at positions 481T, 803G, 590A and 857A of the NAT2 gene were determined by a polymerase chain reaction-restriction fragment length polymorphism assay (PCR-RFLP). RESULTS: The frequency of homozygous fast acetylators did not differ significantly between patients and controls. Compared with the control population, the significant prevalence of slow acetylators in the group of patients with atopic asthma was observed. There was a statistically significant prevalence of subjects with NAT2*5/NAT2*5 and NAT2*5/NAT2*6 genotypes. The risk of an atopic asthma development was 3.4 times greater in slow than in fast acetylators (OR = 3.3657; p <0.000001, 95% CI = 2.1282-5.3228). CONCLUSIONS: These results suggest that NAT2 polymorphism may be involved in the pathogenesis of atopic asthma.