Leukotriene-related Gene Polymorphisms in Patients with Aspirin-intolerant Urticaria and Aspirin-intolerant Asthma: Differing Contributions of ALOX5 Polymorphism in Korean Population.
10.3346/jkms.2005.20.6.926
- Author:
Seung Hyun KIM
1
;
Jeong Hee CHOI
;
J W HOLLOWAY
;
Chang Hee SUH
;
Dong Ho NAHM
;
Eun Ho HA
;
Choon Sik PARK
;
Hae Sim PARK
Author Information
1. Department of Allergy and Rheumatology, Ajou University School of Medicine, Suwon, Korea. hspark@ajou.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Aspirin, Hypersensitivity;
Urticaria;
Polymorphism, Genetic;
Leukotrienes
- MeSH:
Adult;
Arachidonate 5-Lipoxygenase/*genetics;
Aspirin/*adverse effects;
Asthma/etiology/*genetics/metabolism;
Carrier Proteins/genetics;
Case-Control Studies;
Cyclooxygenase 2/genetics;
Female;
Gene Frequency;
Genotype;
Glutathione Transferase/genetics;
Humans;
Leukotrienes/*biosynthesis;
Male;
Membrane Proteins/genetics;
Middle Aged;
Polymorphism, Single Nucleotide;
Research Support, Non-U.S. Gov't;
Urticaria/etiology/*genetics/metabolism
- From:Journal of Korean Medical Science
2005;20(6):926-931
- CountryRepublic of Korea
- Language:English
-
Abstract:
The pathogenesis of aspirin (acetylsalicylic acid, ASA)-intolerant urticaria (AIU) is still poorly understood but it has recently been suggested that it is associated with the overproduction of leukotriene (LT). This is supported by evidence that cyclooxygenase 2 inhibitor is given safely to patients with AIU. The present study was designed to investigate the role of genetic polymorphism of LT related genes in the pathogenesis of AIU via a case-control study. We screened single nucleotide polymorphisms (SNPs) in genes encoding enzymes involved in leukotriene synthesis in the Korean population with AIU (n=101), ASA-intolerant asthma (AIA, n=95) and normal healthy controls (n=123). Genotype was determined by primer extension reactions using the SNapShot ddNTP primer extension kit. Among 8 SNPs of four LT related genes, the polymorphism of ALOX5 at positions of -1708 G>A showed significant difference in genotype frequency between AIU and AIA (p=0.01). Furthermore, there were significant differences observed in the frequencies of two ALOX5 haplotypes between the AIU group and AIA group (p<0.05). However, there were no differences in allele, genotype, or haplotype frequencies of ALOX5 between the AIU group and the normal control group. These results suggested that ALOX5 has a differing contribution in two major clinical pathogenesis related to ASA-sensitivity.
