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COVID-19 是否是良性前列腺增生进展和其相关症状恶化的危险因素?:系统评价。

Is COVID-19 a risk factor for progression of benign prostatic hyperplasia and exacerbation of its related symptoms?: a systematic review.

机构信息

Shiraz Nephro-Urology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.

Department of Urology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.

出版信息

Prostate Cancer Prostatic Dis. 2022 Mar;25(1):27-38. doi: 10.1038/s41391-021-00388-3. Epub 2021 May 18.

DOI:10.1038/s41391-021-00388-3
PMID:34007019
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8129694/
Abstract

BACKGROUND

To explore the potential mechanisms of SARS-CoV-2 in targeting the prostate gland, leading to exacerbation of benign prostatic hyperplasia (BPH) symptoms and greater risks of BPH complications such as acute urinary retention.

METHODS

A categorized and comprehensive search in the literature has been conducted by 10 April 2021 using international databases including PubMed, Embase, Web of Science, Scopus, and Cochrane Library in line with the PRISMA guidelines recommendations. PICO strategy was used to formulate the research question. The following terms were used: urology, COVID-19, coronavirus, BPH, inflammation, androgen receptors, LUTS, IPSS, PSA, and SARS-CoV-2 or a combination of them. Studies with irrelevant purposes and duplicates were excluded. The selected studies were performed on humans and published in English.

RESULTS

The research revealed 89 articles. After title screening and considering exclusion criteria, 52 papers were included for the systematic review. BPH is a common condition affecting older men. SARS-CoV-2 infects the host cell by binding to angiotensin converting enzyme 2 (ACE2). A hyperactivated RAS system during infection with SARS-CoV-2 may lead to activation of pro-inflammatory pathways and increased cytokine release. Thus, this virus can lead to exacerbation of lower urinary tract symptoms (LUTS) and trigger inflammatory processes in the prostate gland. Since androgen receptors (AR) play an important role in the BPH pathophysiology and infection with SARS-CoV-2 may be androgen-mediated, BPH progression and its related symptoms can be a complication of COVID-19 through AR involvement and metabolic disturbances.

CONCLUSIONS

Based on the current findings, SARS-CoV-2 can possibly damage the prostate and worsen BPH and its related LUTS through ACE2 signaling, AR-related mechanisms, inflammation, and metabolic derangement. We encourage future studies to investigate the possible role of COVID-19 in the progression of BPH-related LUTS and examine the prostatic status in susceptible patients with relevant available questionnaires (e.g., IPSS) and serum biomarkers (e.g., PSA).

摘要

背景

探究 SARS-CoV-2 靶向前列腺的潜在机制,导致良性前列腺增生 (BPH) 症状恶化,并增加 BPH 并发症(如急性尿潴留)的风险。

方法

我们于 2021 年 4 月 10 日,按照 PRISMA 指南的建议,通过国际数据库(包括 PubMed、Embase、Web of Science、Scopus 和 Cochrane Library),进行了文献的分类和综合搜索。使用 PICO 策略来制定研究问题。使用了以下术语:泌尿科、COVID-19、冠状病毒、BPH、炎症、雄激素受体、LUTS、IPSS、PSA 和 SARS-CoV-2 或它们的组合。排除了与目的不相关和重复的研究。所选择的研究是在人类中进行的,并以英文发表。

结果

研究共检索到 89 篇文章。经过标题筛选并考虑排除标准后,有 52 篇文章纳入系统评价。BPH 是一种影响老年男性的常见疾病。SARS-CoV-2 通过与血管紧张素转换酶 2(ACE2)结合来感染宿主细胞。感染 SARS-CoV-2 时,RAS 系统过度激活可能导致促炎途径的激活和细胞因子的释放增加。因此,这种病毒可能导致下尿路症状(LUTS)恶化,并引发前列腺的炎症过程。由于雄激素受体(AR)在 BPH 病理生理学中发挥重要作用,并且 SARS-CoV-2 的感染可能是雄激素介导的,因此,BPH 的进展及其相关症状可能通过 AR 参与和代谢紊乱成为 COVID-19 的并发症。

结论

根据目前的发现,SARS-CoV-2 可能通过 ACE2 信号、AR 相关机制、炎症和代谢紊乱对前列腺造成损害,从而使 BPH 及其相关的 LUTS 恶化。我们鼓励未来的研究调查 COVID-19 在 BPH 相关 LUTS 进展中的可能作用,并通过相关的现有问卷(如 IPSS)和血清生物标志物(如 PSA)检查易感患者的前列腺状况。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e574/8129694/939de82ef2c4/41391_2021_388_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e574/8129694/0e67aaffe5ec/41391_2021_388_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e574/8129694/7bb52fc730f0/41391_2021_388_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e574/8129694/f72a61c7e81e/41391_2021_388_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e574/8129694/939de82ef2c4/41391_2021_388_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e574/8129694/0e67aaffe5ec/41391_2021_388_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e574/8129694/7bb52fc730f0/41391_2021_388_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e574/8129694/f72a61c7e81e/41391_2021_388_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e574/8129694/939de82ef2c4/41391_2021_388_Fig4_HTML.jpg

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