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, Peopleís 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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MATERIALS AND METHODS

Search Strategy. A systematic search assembling the following terms: genetic polymorphism, single nucleotide polymorphism, gene mutation, genetic variants, coronary atherosclerosis, myocardial ischemia, acute coronary syndrome, coronary artery disease, myocardial infarction, ischemic heart disease, TNFRSF11B, osteoprotegerin, was conducted in PubMed, Web of Science, Cochrane Library, Chinese National Knowledge Infrastructure (CNKI) and Chinese Wan Fang databases up to May 1 2017 to identify all potentially relevant studies. Hand-searching was carried out to determine other potential eligible studies through scanning the references cited in the retrieved articles. The full-text articles were further reviewed to determine whether they were included in the final analysis strictly based on eligibility criteria. If two reviewers disagreed, all the authors critically evaluated the studies to judge of the inclusion or exclusion of a certain study. Eligibility Criteria. All the eligible articles were supposed to meet the following major inclusion criteria: i) assessment of the association between OPG gene polymorphisms and CAD; ii) case-control or cohort studies; iii) data provided by articles about allele frequency should be sufficient for calculating genotypic odds ratio (OR) with corresponding to 95% confidence interval (95% CI) in cases and controls. Moreover, only when a single nucleotide polymorphism (SNP) in the OPG gene was reported by at least two articles would it be analyzed by meta-analysis. Studies were excluded when they were i) duplicated data; ii) case report, review articles and editorial comment. The diagnosis of the CAD case was based on the WHO criteria for CAD as previously described (stenosis ≥50.0% of the diameter in at least one major coronary artery based on computerassisted assessments) [17]. All healthy control subjects were identified according to patient history, serum biochemistry examination and electrocardiogram (ECG) test. Data Extraction. Data extraction was performed independently by two authors using a standardized data extraction form including following elements: 1) authorís name, year of publication; 2) patient characteristics of each group; 3) number of participants in case and control groups; 4) study type; 5) genotyping method; 6) p value of Hardy-Weinberg equilibrium (HWE) test in the control; 7) OR and 95% CI for association with CAD. Assessment of the quality of studies was performed using the Newcastle- Ottawa Scale (NOS) as previously described [18]. Briefly, two authors of this article separately evaluated the qualities based on eight items and scored the studies from 0 to 9 points. Studies with a score not less than seven points were considered to be of high quality. Discrepancy was resolved as described above. Statistical Analyses. First, the genotype frequencies of the OPG gene polymorphism among the controls of all included studies were assessed under HWE using a χ2 goodness- of-fit test. Odds ratios with corresponding 95% CIs were used to estimate the strength of association between OPG gene polymorphisms and CAD. The between-study heterogeneity across all eligible comparisons was tested by the χ2-based Q statistic. Heterogeneity was considered significant when the p value was less than 0.10. When heterogeneity existed, the random effects model was performed to calculate the pooled OR of each eligible study, otherwise, the fixed effect model was used. Generally, we assessed the association between the OPG gene polymorphism and CAD under five genetic models: allele, homozygote, heterozygote, dominant and recessive models. Sensitivity analysis was conducted through omitting one study at a time to examine its influence on the overall estimate to evaluate the stability of the meta-analysis. Publication bias was also analyzed using the Eggerís linear regression test and funnel plots and publication bias was considered present when the p value was less than 0.05. All statistical analyses were done using STATA version 11.0 (STATA Corporation, College Station, TX, USA). All p values were two-tailed.



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