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慢性阻塞性肺疾病患者能否从肾素-血管紧张素系统抑制剂中获益?一项荟萃分析。

Could patients with chronic obstructive pulmonary disease benefit from renin angiotensin system inhibitors? A meta-analysis.

机构信息

Department of Basic Medicine, Jiangsu Vocational College of Medicine, Yancheng, China.

Department of Respiratory and Critical Care Medicine, Baoshan Branch, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China.

出版信息

BMJ Open Respir Res. 2023 Feb;10(1). doi: 10.1136/bmjresp-2022-001569.

DOI:10.1136/bmjresp-2022-001569
PMID:36828646
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9972452/
Abstract

BACKGROUND

Chronic obstructive pulmonary disease (COPD) is considered related to chronic systemic inflammation. Renin angiotensin system (RAS) inhibitor, exerting an anti-inflammatory action in many systems, has been demonstrated relevant to the pathogenesis of COPD. However, the association between RAS inhibitor use and prognosis of patients with COPD remains controversial. Therefore, we conducted a meta-analysis and systematic review to summarise current evidence.

MATERIAL AND METHODS

Databases, including Medline, Embase, Web of Science and Cochran Library, were searched for eligible studies by the end of 30 September 2022. Observational studies or randomised controlled trials (RCTs) that investigated the association of RAS inhibitor use with prognosis of COPD (mortality or risk of acute exacerbation) were selected. The Newcastle-Ottawa Scale was used for quality assessment of observational studies, while the Cochrane risk-of-bias tool was used to assess the quality of RCTs. Statistical analyses were performed using Stata V.15. We selected relative risk (RR) with 95% CI as the effect measure. Heterogeneity was assessed by I-squared (I) statistics. The funnel plot was used for visual assessment of publication bias.

RESULTS

A total of 20 studies with 5 51 649 subjects were included in the meta-analysis. The overall analysis indicated that RAS inhibitor use decreased the risk of death in patients with COPD (RR: 0.69, 95% CI: 0.61 to 0.78). Subgroup analyses were conducted according to comorbidities, race and type of RAS inhibitors, and the results kept consistent. However, in the pooled analysis of prospective studies, RAS inhibitor use did not significantly decrease the mortality (RR: 0.89, 95% CI: 0.78 to 1.02). Additionally, the risk of exacerbations of COPD did not decrease in patients who were prescribed RAS inhibitors (RR: 0.99, 95% CI: 0.80 to 1.23). The funnel plot indicated significant publication bias.

CONCLUSION

RAS inhibitor use seemed to be associated with a reduction of mortality in patients with COPD. However, the available evidence is weak due to potential biases from retrospective studies and the heterogeneity across included studies.

摘要

背景

慢性阻塞性肺疾病(COPD)被认为与慢性全身炎症有关。肾素-血管紧张素系统(RAS)抑制剂在许多系统中具有抗炎作用,与 COPD 的发病机制有关。然而,RAS 抑制剂的使用与 COPD 患者的预后之间的关系仍存在争议。因此,我们进行了一项荟萃分析和系统评价,以总结目前的证据。

材料和方法

截至 2022 年 9 月 30 日,通过 Medline、Embase、Web of Science 和 Cochrane 图书馆等数据库搜索了符合条件的研究。选择了研究 RAS 抑制剂使用与 COPD 预后(死亡率或急性加重风险)之间关系的观察性研究或随机对照试验(RCT)。采用纽卡斯尔-渥太华量表评估观察性研究的质量,采用 Cochrane 偏倚风险工具评估 RCT 的质量。采用 Stata V.15 进行统计学分析。我们选择相对风险(RR)和 95%置信区间(CI)作为效应量。采用 I 平方(I)统计量评估异质性。采用漏斗图评估发表偏倚的情况。

结果

共纳入 20 项研究,涉及 551649 名患者。总体分析表明,RAS 抑制剂的使用降低了 COPD 患者的死亡风险(RR:0.69,95%CI:0.61 至 0.78)。根据合并症、种族和 RAS 抑制剂类型进行亚组分析,结果保持一致。然而,在前瞻性研究的汇总分析中,RAS 抑制剂的使用并不能显著降低死亡率(RR:0.89,95%CI:0.78 至 1.02)。此外,使用 RAS 抑制剂的 COPD 患者急性加重的风险并未降低(RR:0.99,95%CI:0.80 至 1.23)。漏斗图表明存在显著的发表偏倚。

结论

RAS 抑制剂的使用似乎与 COPD 患者的死亡率降低有关。然而,由于来自回顾性研究的潜在偏倚以及纳入研究之间的异质性,现有证据较弱。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc9/9972452/c4cc70ee43a7/bmjresp-2022-001569f06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc9/9972452/0f4de428f86d/bmjresp-2022-001569f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc9/9972452/8431a291a6fe/bmjresp-2022-001569f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc9/9972452/8e0b7a943c19/bmjresp-2022-001569f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc9/9972452/4eaff0d70e8a/bmjresp-2022-001569f04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc9/9972452/15cf857d9b73/bmjresp-2022-001569f05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc9/9972452/c4cc70ee43a7/bmjresp-2022-001569f06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc9/9972452/0f4de428f86d/bmjresp-2022-001569f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc9/9972452/8431a291a6fe/bmjresp-2022-001569f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc9/9972452/8e0b7a943c19/bmjresp-2022-001569f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc9/9972452/4eaff0d70e8a/bmjresp-2022-001569f04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc9/9972452/15cf857d9b73/bmjresp-2022-001569f05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc9/9972452/c4cc70ee43a7/bmjresp-2022-001569f06.jpg

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