ASSOCIATION BETWEEN OSTEOPROTEGERIN GENE POLYMORPHISMS AND RISK OF CORONARY ARTERY DISEASE: A SYSTEMATIC REVIEW AND META-ANALYSIS
Jia P, Wu N, Jia D, Sun Y
*Corresponding Author: Professor Dalin Jia and/or Professor Yingxian Sun, Department of Cardiology, The First Affiliated Hospital of China Medical University, 155th North Nanjing Street, Heping District, Shenyang 110001, Liaoning Province, People’s Republic of China. Tel: +86-242-326-9477. Fax: +86-242-326-9477. Email: jdl2001@126.com and/or yxsun@mail.cmu.edu.cn
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RESULTS

Results of the Literature Search. As shown in Figure.1, 36 potentially eligible records were initially identified through literature search. Thirty articles were excluded, including seven articles that were duplicated, five articles that were reviews, 12 articles that did not involve CAD, four articles that did not conform to the diagnostic criteria of CAD, one article that lacked normal controls, and one article that did not provide sufficient data for the distribution of the genotype. Finally, six articles in accordance with the inclusion criteria were included in this meta-analysis [12-16,19]. To be specific, two studies involved the G209A polymorphism, three studies with T245G polymorphism, three studies with T950C polymorphism, and five studies with G1181C polymorphism. Characteristics of Included Studies. The characteristics of the included studies are summarized in Table 1. Overall, four studies were conducted in Asians, and the other two studies were carried out in Caucasians. The polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method was used to detect the gene polymorphisms in five out of six studies. The average score of NOS was at 9. The genotype distribution of the controls in all studies was consistent with HWE. Quantitative Data Synthesis. Meta-analysis of the G209A polymorphism was involved with two studies consisting of 215 CAD cases and 98 controls. There was no association between the G209A polymorphism and the risk of CAD when pooling all the data in the meta-analysis (AA/AG vs. GG: OR = 1.005, 95% CI = 0.564-1.792, p = 0.986) (Figure 2A) (Table 2). For the T245G polymorphism, three studies with 393 CAD cases and 410 controls were included for final meta-analysis, but the results showed no relationship between the T245G polymorphism and the risk of CAD either (TT/TG vs. GG: OR = 0.664, 95% CI = 0.247-1.785, p = 0.417) (Figure 2B) (Table 2). For the T950C polymorphism, 1105 CAD cases and 906 controls were included in the meta-analysis. A significant association was found between the T950C polymorphism and risk of CAD under the dominant model (CC/CT vs. TT: OR = 1.327, 95% CI = 1.090-1.617, p = 0.005) (Figure 2C), allele model (C vs. T: OR = 1.264, 95% CI = 1.108- 1.442, p <0.001), homozygote model (CC vs. TT: OR = 1.615, 95% CI = 1.242-2.100, p <0.001), recessive model (CC vs. CT/TT: OR = 1.376, 95% CI = 1.097-1.726, p = 0.006) (Table 2). Meta-analysis of the G1181C polymorphism was involved with five studies consisting of 1137 CAD cases and 1024 controls and the results indicated that the G1181C polymorphism was significantly associated with the risk of CAD under the dominant model (CC/CG vs. GG: OR = 1.268, 95% CI = 1.064-1.511, p = 0.008) (Figure 4D). In addition, a statistically significant association also existed between the G1181C polymorphism and risk of CAD under the heterozygote model (CG vs. GG: OR = 1.243, 95% CI = 1.027-1.504, p = 0.026) (Table 2). Sensitivity Analysis and Publication Bias. The result of the sensitivity analysis showed that the pooled ORs of the G209A, T245G, T950C and G1181C polymorphisms were not considerably affected by eliminating any individual study (Figure 3). The funnel plots were symmetrical by visual inspection (Figure 4) and Egger’s test also suggested no publication bias (p >0.05). These results confirmed that this meta-analysis was robust.



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