性激素与肺纤维化关系的元分析。

Postgraduate medicine Pub Date : 2024-06-01 Epub Date: 2024-08-07 DOI:10.1080/00325481.2024.2373683
Ying Chen, Jiaxin Zhong, Zixin Cai, Zhenkun Xia, Bei Qing, Yunchang Yuan, Jingjing Zhang
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引用次数: 0

摘要

研究背景本研究旨在通过对以前发表的研究进行荟萃分析,探讨性激素与肺纤维化风险之间的关系:我们对 PubMed、Embase、Cochrane Library 和 Web of Science 数据库进行了全面检索,以找到截至 2024 年 4 月发表的相关研究。我们纳入了报告性激素与肺纤维化风险之间关系的研究。采用随机效应模型计算标准化平均差(SMD)和 95% 置信区间(CI):本荟萃分析最终纳入了共 10 篇文章,涉及 1371 名患者。根据对纳入研究的评估,观察到硫酸脱氢表雄酮(DHEA-S)的水平(汇总 SMD:-0.72,95% CI:-1.21 至 -0.24,p p p 结论:这项荟萃分析表明,DHEA-S、睾酮和雌激素水平的降低可能是肺纤维化的潜在危险因素。目前迫切需要更多的研究来证实这种关联,并探索其潜在的生物学机制。临床医生应认识到性激素在肺纤维化病因学中的潜在影响,并在患者管理过程中考虑这方面的因素。
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Meta-analysis of the association between sex hormones and pulmonary fibrosis.

Background: This study aimed to investigate the association between sex hormones and the risk of pulmonary fibrosis by conducting a meta-analysis of previously published studies.

Methods: We executed a comprehensive search of the PubMed, Embase, Cochrane Library, and Web of Science databases to locate pertinent studies published up to April 2024. We included studies that reported the association between sex hormones and the risk of pulmonary fibrosis. Standardized mean difference (SMD) with 95% confidence intervals (CIs) were calculated using a random-effects model.

Results: A total of 10 articles, encompassing 1371 patients, were finally incorporated in this meta-analysis. Based on the evaluation of the included studies, it was observed that the levels of dehydroepiandrosterone sulfate (DHEA-S) (pooled SMD: -0.72, 95% CI: -1.21 to -0.24, p < 0.001), testosterone (pooled SMD: -1.25, CI: -2.39 and -0.11, p < 0.001) and estrogen (pooled SMD: -0.56, 95% CI: -0.96 to -0.15, p < 0.001) were significantly lower in patients with pulmonary fibrosis, whereas the levels of luteinizing hormone (LH) remained unaffected. Publication bias was ruled out through funnel plots.

Conclusion: This meta-analysis indicates that reduced levels of DHEA-S, testosterone, estrogen may serve as potential risk factors for pulmonary fibrosis. There is a pressing need for additional studies to confirm this association and explore the underlying biological mechanisms. Clinicians should recognize the potential influence of sex hormones in the etiology of pulmonary fibrosis and consider this aspect during the patient management process.

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