The Correlation Analysis of Two Common Polymorphisms in STAT6 Gene and the Risk of Asthma: A Meta-Analysis

BACKGROUND Several studies have reported that the GT dinucleotide repeat length polymorphism and the G2964A polymorphism in signal transducer and activator of transcriptional factor 6 gene are associated with asthma susceptibility, but others have conflicting results. Our meta-analysis aimed to elucidate the emerging paradigms. METHODS We searched PUBMED, EMBASE, ISI web of knowledge, Chinese National Knowledge Infrastructure, and Wanfang databases. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were used to evaluate the strength of association. We applied Bonferroni step-down and Benjamini-Hochberg step-up methods to adjust the values for multiple comparisons. RESULTS A total of 12 individual studies in 11 articles were included in the meta-analysis. For GT repeat polymorphism, the S allele had approximately 45% increased risk of asthma (S vs. L: OR  =  1.45, 95% CI  =  1.22-1.71, P(UNCORRECTED) < 0.001, P(Bon) < 0.001, P(FDR) < 0.001). Further analysis indicated that GT13 and GT14 contributed to asthma risk, whereas GT15 and GT16 were protective (GT13 vs. GT15: OR  =  1.38, 95% CI  =  1.16-1.65, P(UNCORRECTED ) =  0.001, P(Bon) =  0.005, P(FDR) =  0.002). Similar results were obtained in the subgroup analysis of Asian population. G2964A polymorphism analysis showed that the AA genotype moderately increased the risk of asthma by 47% compared with the GG genotype (OR  =  1.47, p  =  0.068) in Chinese population, whereas the 2964A allele moderately increased the risk of asthma in Chinese population by 18% (2964A vs. 2964G: OR  =  1.18, p  =  0.08). However, none of the associations reached statistically significant levels particularly after correction for multiple testing. CONCLUSIONS This meta-analysis suggests that S allele (GT13 and GT14) of the GT repeat polymorphism confers significant risks to asthma. However, the G2964A polymorphism does not have an association with the susceptibility to asthma.