Department of Respiratory Medicine, The Third People's Hospital of Anji, China.
Emergency Department, The People's Hospital of Anji, China.
J Renin Angiotensin Aldosterone Syst. 2020 Jan-Mar;21(1):1470320319900039. doi: 10.1177/1470320319900039.
The purpose of the study was to investigate the association between angiotensin-converting enzyme gene insertion/deletion polymorphism and high-altitude pulmonary edema.
A systematic search for relevant literature was performed in MEDLINE, CNKI, and EMBASE. The pooled odds ratios and their corresponding 95% confidence intervals were calculated in STATA 12.0 software.
Seven studies, with a total of 304 patients and 564 controls, qualified for the inclusion in the analysis. There was no significant association between angiotensin-converting enzyme insertion/deletion polymorphism and high-altitude pulmonary edema risk in the total population (DD vs II: odds ratio=1.07, 95% confidence interval 0.52-2.24; DI vs II: odds ratio=1.12, 0.85-1.49; dominant model: odds ratio=1.07, 0.83-1.40; recessive model: odds ratio=0.96, 0.53-1.77). Subgroup analysis according to race also revealed no significant correlation between angiotensin-converting enzyme gene insertion/deletion polymorphism and high-altitude pulmonary edema.
Our findings suggest that angiotensin-converting enzyme insertion/deletion polymorphism does not contribute to the risk of high-altitude pulmonary edema. Larger, well-designed studies are required to further validate these results.
研究的目的是探讨血管紧张素转换酶基因插入/缺失多态性与高原肺水肿的关系。
在 MEDLINE、CNKI 和 EMBASE 中进行了系统的文献检索。使用 STATA 12.0 软件计算汇总的优势比及其相应的 95%置信区间。
共有 7 项研究，总计 304 例患者和 564 例对照符合纳入分析的标准。在总体人群中，血管紧张素转换酶插入/缺失多态性与高原肺水肿风险之间没有显著关联（DD 与 II 相比：优势比=1.07，95%置信区间 0.52-2.24；DI 与 II 相比：优势比=1.12，0.85-1.49；显性模型：优势比=1.07，0.83-1.40；隐性模型：优势比=0.96，0.53-1.77）。按种族进行的亚组分析也显示血管紧张素转换酶基因插入/缺失多态性与高原肺水肿之间没有相关性。
我们的研究结果表明，血管紧张素转换酶插入/缺失多态性与高原肺水肿的风险无关。需要更大、设计更好的研究来进一步验证这些结果。
