作者: Guoping HU , Zhe SHI , Jinxing HU , Guoming ZOU , Gongyong PENG
DOI: 10.1111/J.1440-1843.2008.01356.X
关键词:
摘要: Background and objective: COPD is a complex polygenic disease in which gene–environment interactions are very important. The gene encoding microsomal epoxide hydrolase (EPHX1) one of several candidate loci for pathogenesis highly polymorphic. Based χ on the polymorphisms EPHX1 (tyrosine/histidine 113, histidine/arginine 139), population can be classified into four groups putative phenotypes (fast, normal, slow slow). A number studies have investigated association between genotypes susceptibility different populations, with inconsistent results. systematic review meta-analysis published data was performed to gain clearer understanding this association. Methods: MEDLINE database searched case–control from 1966 August 2007. Data were extracted pooled odds ratios (OR) 95% confidence intervals (CI) calculated. Results: Sixteen eligible studies, comprising 1847 patients 2455 controls, included meta-analysis. result showed that 113 mutant homozygote significantly associated an increased risk (OR 1.59, CI: 1.14–2.21). Subgroup analysis supported Asian population, but not Caucasian population. When limited only larger-sample-size controls Hardy–Weinberg equilibrium smokers/ex-smokers, results conclusion. 139 heterozygote protected against development other types COPD. activity phenotype fast protective factor developing However, population. Conclusions: genetic contributors populations. overall susceptibility.