In:
Pharmacogenomics, Future Medicine Ltd, Vol. 11, No. 7 ( 2010-07), p. 951-958
Abstract:
Aims: Cysteinyl leukotrienes are inactivated by acetyl coenzyme A-dependent N-acetyltransferase (NAT). Thus, functional alterations of the NAT gene may contribute to the risk of aspirin-intolerant asthma. Materials & methods: Asthmatics (n = 438) were categorized into aspirin-intolerant asthma (15% or greater decrease in the forced expiratory volume in 1 s or cutaneous reactions, n = 170) or aspirin-tolerant asthma (n = 268) groups. In total, 14 polymorphisms of the NAT2 gene were genotyped by a single-base extension method. Results: The distributions of all loci of the 14 SNPs were in Hardy–Weinberg equilibrium (p 〉 0.05). Among the 14 SNPs, six common SNPs (minor allele frequency 〉 5%) in a Korean population were used for haplotype construction and further statistical analysis. The logistic regression analysis demonstrated that NAT2 -9246G 〉 C and haplotype 2 (TCACGG) were significantly associated with the risk of aspirin-intolerant asthma. The rare allele frequencies of the SNP and Ht2 were significantly higher in the aspirin-intolerant asthma group than in the aspirin-tolerant asthma group (p corr = 0.03 and p corr = 0.02 in codominant model). Conclusion: In a large genetic epidemiology study of aspirin-intolerant asthma in a Korean population, genetic polymorphisms of NAT2 were found to be related to a risk of aspirin hypersensitivity among asthmatics.
Type of Medium:
Online Resource
ISSN:
1462-2416
,
1744-8042
Language:
English
Publisher:
Future Medicine Ltd
Publication Date:
2010
SSG:
15,3
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