Lack of association between interleukin-1 receptor antagonist gene 86-bp VNTR polymorphism and ischemic stroke: A meta-analysis. Issue 31 (August 2018)

• Record Type: Journal Article
• Authors: Yang, Yujiao; Wu, Wenhui; Wang, Long; Ding, Yi
• Other Names: Bush. Eric section editor.
• Is Part Of: Medicine. Volume 97:Issue 31(2018)
• Publication Date: 2018-08
• Subjects: interleukin-1 receptor antagonist -- ischemic stroke -- meta-analysis -- variable number tandem repeat; Medicine -- Periodicals; Medicine -- Periodicals; Médecine -- Périodiques; Geneeskunde; Medicine; Periodicals; Periodicals; 610.5
• DOI: 10.1097/MD.0000000000011750
• Languages: English
• ISSNs: 0025-7974

Abstract

Abstract: Objective: The results of published studies which examined the association between variable number tandem repeat (VNTR) polymorphism of interleukin-1 receptor antagonist (IL-1RN) and ischemic stroke (IS) are conflicting. Thus, we performed a meta-analysis to examine the potential association between IL-1RN VNTR polymorphism and IS risk. Methods: A systematic literature search of PubMed, Embase, Medline, Web of Science, Cochrane Library, Chinese Biomedical Literature Database, Chinese National Knowledge Infrastructure, CQVIP, and WANFANG Database identified 10 studies with 2331 cases and 3335 controls. The pooled odds ratio (OR) with 95% confidence interval (95% CI) was calculated to evaluate the strength of the association. Subgroup analysis and meta-regression analysis were used to investigate the potential sources of heterogeneity. Begg funnel plots were used to explore the publication bias. Results: In this study, no enough proof was found to prove the association between IL-1RN 86-bp VNTR polymorphism and IS risk with random-effects model in the homozygous model (1/1 vs 2/2, OR = 0.97, 95% CI = 0.50–1.87, P heterogeneity = .00), the heterozygous model (1/2 vs 2/2, OR = 0.64, 95% CI = 0.41–1.01, P heterogeneity = .10), the dominant model (1/1 + 1/2 vs 2/2, OR = 0.85, 95% CI = 0.51–1.42, P heterogeneity = .02), the recessive model (1/1 vs 1/2 + 2/2, OR = 0.69, 95% CI = 0.46–1.03, P heterogeneity = .00), and allelic model (1 vs 2, OR = 1.24, 95% CI = 0.89–1.74, P heterogeneity = .00). A marginally significant negative association was observed between IL-1RN 86-bp VNTR polymorphism and IS risk in the heterozygous model in the fixed-effects model (1/2 vs 2/2, OR = 0.71, 95% CI = 0.53–0.95, P heterogeneity = .10). In subgroup analyses, similar association was found in the group whose control size was lower than 300. Conclusion: In conclusion, our results suggested that there was no sufficient evidence to support the association between IL-1RN 86-bp VNTR polymorphism and IS. Further large epidemiologic studies need to be done to confirm these findings. Abstract : Supplemental Digital Content is available in the text