Yadong Song1, Zhilei Shan2, Cheng Luo2, Cuixin Kang3, Yong Yang3, Ping He3, Shoudao Li3, Liangkai Chen2, Xiaoming Jiang4, Liegang Liu5. 1. Wuhan Institute for Food and Cosmetic Control, 430012, Wuhan, People's Republic of China; Department of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, Tongji Medical College, Huazhong University of Science and Technology, 430030 Wuhan, People's Republic of China. 2. Ministry of Education Key Laboratory of Environment and Health, School of Public Health, Tongji Medical College, People's Republic of China; Department of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, Tongji Medical College, Huazhong University of Science and Technology, 430030 Wuhan, People's Republic of China. 3. Wuhan Institute for Food and Cosmetic Control, 430012, Wuhan, People's Republic of China. 4. Wuhan Institute for Food and Cosmetic Control, 430012, Wuhan, People's Republic of China. Electronic address: jxm_01@163.com. 5. Ministry of Education Key Laboratory of Environment and Health, School of Public Health, Tongji Medical College, People's Republic of China; Department of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, Tongji Medical College, Huazhong University of Science and Technology, 430030 Wuhan, People's Republic of China. Electronic address: lgliu@mails.tjmu.edu.cn.
Abstract
BACKGROUND: The association between glutathione S-transferase T1 (GSTT1) null polymorphism and coronary heart disease (CHD) is inconsistent among studies, and data on the GSTT1 null genotype-smoking interplay in CHD is lacking. We conducted this meta-analysis to investigate the relationship between GSTT1 null polymorphism and CHD and to assess the potential interaction between GSTT1 null genotype and smoking. METHODS: PubMed and EMBASE databases were searched up to 27 January 2016 using the appropriate terms. Odds ratios were pooled using either fixed-effects or random-effects models. RESULTS: Twenty-nine articles including 31 studies with 15,004 cases and 35,597 controls were eligible. The random-effects model showed that the GSTT1 null genotype was associated with increased CHD risk (OR=1.213, 95%CI: 1.004-1.467; I2=90.4%). After excluding 10 studies detected by Galbraith plot, the fixed effects summary estimate also showed an increased risk of CHD (OR=1.14, 95% CI: 1.06-1.22; I2=27.7%). A case-only analysis including eight studies showed a statistically significant positive interaction between GSTT1 null polymorphism and smoking status on CHD (OR=1.34, 95% CI: 1.09-1.64; I2=0%). Sensitivity analyses further supported the associations. No publication bias was observed. CONCLUSIONS: This meta-analysis suggests that GSTT1 null polymorphism is associated with the risk of CHD. To our knowledge, this is the first meta-analysis to prove a positive effect of the interaction between GSTT1 null genotype and smoking status on the risk of CHD. Future studies with detailed individual information are needed to confirm our findings.
BACKGROUND: The association between glutathione S-transferase T1 (GSTT1) null polymorphism and coronary heart disease (CHD) is inconsistent among studies, and data on the GSTT1 null genotype-smoking interplay in CHD is lacking. We conducted this meta-analysis to investigate the relationship between GSTT1 null polymorphism and CHD and to assess the potential interaction between GSTT1 null genotype and smoking. METHODS: PubMed and EMBASE databases were searched up to 27 January 2016 using the appropriate terms. Odds ratios were pooled using either fixed-effects or random-effects models. RESULTS: Twenty-nine articles including 31 studies with 15,004 cases and 35,597 controls were eligible. The random-effects model showed that the GSTT1 null genotype was associated with increased CHD risk (OR=1.213, 95%CI: 1.004-1.467; I2=90.4%). After excluding 10 studies detected by Galbraith plot, the fixed effects summary estimate also showed an increased risk of CHD (OR=1.14, 95% CI: 1.06-1.22; I2=27.7%). A case-only analysis including eight studies showed a statistically significant positive interaction between GSTT1 null polymorphism and smoking status on CHD (OR=1.34, 95% CI: 1.09-1.64; I2=0%). Sensitivity analyses further supported the associations. No publication bias was observed. CONCLUSIONS: This meta-analysis suggests that GSTT1 null polymorphism is associated with the risk of CHD. To our knowledge, this is the first meta-analysis to prove a positive effect of the interaction between GSTT1 null genotype and smoking status on the risk of CHD. Future studies with detailed individual information are needed to confirm our findings.
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