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首页> 外文期刊>Journal of Renin-Angiotensin-Aldosterone System >Association of angiotensin-converting enzyme gene insertion/deletion polymorphism with high-altitude pulmonary oedema: a meta-analysis
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Association of angiotensin-converting enzyme gene insertion/deletion polymorphism with high-altitude pulmonary oedema: a meta-analysis

机译:血管紧张素转换酶基因插入/缺失多态性与高海拔肺水肿的关联:一项荟萃分析

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Background and objective: High-altitude pulmonary oedema (HAPE) is a non-cardiogenic hydrostatic oedema involving a genetic component. Considering the low incidence of HAPE, sample sizes in current reports are relatively limited. We aimed to assess the association between the angiotensin-converting enzyme (ACE) I/D polymorphism and HAPE via a meta-analysis of published and unpublished data. Materials and methods: We searched PubMed, CBM, CNKI, and Cochrane Library Database before 20 November 2010. A random-effects model was applied (STATA) and study quality was assessed in duplicate. Results: A total of five studies including 305 cases and 662 controls were meta-analysed. The summary odds ratio (OR) indicated that no significant differences in risk of developing HAPE were found between carriers of ACE D and I alleles (OR = 1.20; 95% confidence interval (CI), 0.98–1.48; p = 0.084). Lack of association persisted for genotypes under the recessive mode. However, genotype association under the dominant mode showed D allele carriers significantly conferred a 1.55-fold increased HAPE risk compared with II genotype carriers (95% CI, 1.15–2.08; p = 0.004). Funnel plot and Egger’s test suggested no evidence of publication bias. Conclusions: Our results supported the notion that ACE D allele carriers were at significant increased risk of developing HAPE.
机译:背景与目的:高原肺水肿(HAPE)是一种非心源性静水性水肿,涉及遗传成分。考虑到HAPE的发生率低,当前报告中的样本量相对有限。我们旨在通过对已发表和未发表数据的荟萃分析来评估血管紧张素转换酶(ACE)I / D多态性与HAPE之间的关联。材料和方法:我们在2010年11月20日之前搜索PubMed,CBM,CNKI和Cochrane图书馆数据库。应用了随机效应模型(STATA),并一式两份地评估了研究质量。结果:荟萃分析了总共五项研究,包括305例病例和662例对照。汇总比值比(OR)表明,ACE D和I等位基因携带者之间发展HAPE的风险没有显着差异(OR = 1.20; 95%置信区间(CI)为0.98-1.48; p = 0.084)。在隐性模式下,基因型缺乏关联。但是,显性模式下的基因型关联显示,与II型基因型携带者相比,D等位基因携带者显着提高了HAPE风险1.55倍(95%CI,1.15-2.08; p = 0.004)。漏斗图和Egger的检验表明,没有证据表明发表有偏见。结论:我们的结果支持了ACE D等位基因携带者罹患HAPE的风险显着增加的观点。

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