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Association analysis of N-acetyl transferase-2 polymorphisms with aspirin intolerance among asthmatics.

Authors: Kim, JM  Park, BL  Park, SM  Lee, SH  Kim, MO  Jung, S  Lee, EH  Uh, ST  Park, JS  Choi, JS  Kim, YH  Kim, MK  Choi, IS  Cho, SH  Choi, BW  Park, HS  Chang, HS  Shin, HD  Park, CS 
Citation: Kim JM, etal., Pharmacogenomics. 2010 Jul;11(7):951-8.
Pubmed: (View Article at PubMed) PMID:20602614
DOI: Full-text: DOI:10.2217/pgs.10.65

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.


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CRRD Object Information
CRRD ID: 5131600
Created: 2011-05-04
Species: All species
Last Modified: 2011-05-04
Status: ACTIVE


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