Yadong Song1,2, Xiaoli Liu1,2, Cheng Luo3,4, Liangkai Chen3,4, Lin Gong1,2, Hanbin Yu1,2, Bin Wang1,2, Ernan Liu1,2, Huiqiong Xu1,2, Jiansheng Liang1,2. 1. Department of Disinfection and Pest Control, Wuhan Centers for Disease Prevention and Control, Wuhan, Hubei, China. 2. Wuhan Healthcare-associated Infection Management Quality Control Center, Wuhan, Hubei, China. 3. Department of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, Tongji Medical College, Hua Zhong University of Science and Technology, Wuhan, People's Republic of China. 4. Ministry of Education Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Wuhan, People's Republic of China.
Abstract
BACKGROUND: Numerous case-control studies have investigated the association between GSTP1 Ile105Val polymorphism and CHD risk, but the results from published studies were inconclusive. The present meta-analysis was performed to derive a more precise estimation. METHODS: PubMed, EMBASE, and Web of Science database searches were conducted to retrieve relevant articles. RESULTS: Ultimately, 5,451 CHD cases and 5,561 controls from 15 studies were included. Pooled analysis did not yield any statistically significant association between GSTP1 Ile105Val polymorphism and CHD risk for the overall population (Val vs. Ile: OR, 1.05; 95% CI, 0.93 to 1.18; Val/Val vs. Ile/Ile: OR, 1.09; 95% CI, 0.83 to 1.42; Val/Ile vs. Ile/Ile: OR, 1.09; 95% CI, 0.93 to 1.28; Val/Val vs. Val/Ile+Ile/Ile: OR, 1.04; 95% CI, 0.83 to 1.30; Val/Val+Val/Ile vs. Ile/Ile: OR, 1.14; 95% CI, 0.97 to 1.33). Subgroup analyses and sensitivity analyses indicated that GSTP1 Ile105Val polymorphism was still not associated with an increased risk of CHD. After excluding studies detected by Galbraith plots as major sources of heterogeneity, these relationships were still not significant. CONCLUSIONS: The overall results did not reveal a major role of the GSTP1 Ile105Val polymorphism in modulating CHD risk. Well-designed studies with large sample sizes are needed to validate our findings and explore the possible gene-gene or gene-environment interactions.
BACKGROUND: Numerous case-control studies have investigated the association between GSTP1Ile105Val polymorphism and CHD risk, but the results from published studies were inconclusive. The present meta-analysis was performed to derive a more precise estimation. METHODS: PubMed, EMBASE, and Web of Science database searches were conducted to retrieve relevant articles. RESULTS: Ultimately, 5,451 CHD cases and 5,561 controls from 15 studies were included. Pooled analysis did not yield any statistically significant association between GSTP1Ile105Val polymorphism and CHD risk for the overall population (Val vs. Ile: OR, 1.05; 95% CI, 0.93 to 1.18; Val/Val vs. Ile/Ile: OR, 1.09; 95% CI, 0.83 to 1.42; Val/Ile vs. Ile/Ile: OR, 1.09; 95% CI, 0.93 to 1.28; Val/Val vs. Val/Ile+Ile/Ile: OR, 1.04; 95% CI, 0.83 to 1.30; Val/Val+Val/Ile vs. Ile/Ile: OR, 1.14; 95% CI, 0.97 to 1.33). Subgroup analyses and sensitivity analyses indicated that GSTP1Ile105Val polymorphism was still not associated with an increased risk of CHD. After excluding studies detected by Galbraith plots as major sources of heterogeneity, these relationships were still not significant. CONCLUSIONS: The overall results did not reveal a major role of the GSTP1Ile105Val polymorphism in modulating CHD risk. Well-designed studies with large sample sizes are needed to validate our findings and explore the possible gene-gene or gene-environment interactions.
Authors: Ning Ding; Xin Wang; Marc G Weisskopf; David Sparrow; Joel Schwartz; Howard Hu; Sung Kyun Park Journal: PLoS One Date: 2016-09-01 Impact factor: 3.240