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2019冠状病毒病危重症患者血浆血管紧张素II水平升高。

Plasma Angiotensin II Is Increased in Critical Coronavirus Disease 2019.

作者信息

Camargo Rafael L, Bombassaro Bruna, Monfort-Pires Milena, Mansour Eli, Palma Andre C, Ribeiro Luciana C, Ulaf Raisa G, Bernardes Ana Flavia, Nunes Thyago A, Agrela Marcus V, Dertkigil Rachel P, Dertkigil Sergio S, Araujo Eliana P, Nadruz Wilson, Moretti Maria Luiza, Velloso Licio A, Sposito Andrei C

机构信息

Obesity and Comorbidities Research Center, University of Campinas, Campinas, Brazil.

Department of Internal Medicine, School of Medical Sciences, University of Campinas, Campinas, Brazil.

出版信息

Front Cardiovasc Med. 2022 Jun 24;9:847809. doi: 10.3389/fcvm.2022.847809. eCollection 2022.

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) employs angiotensin-converting enzyme 2 (ACE2) as its receptor for cell entrance, and studies have suggested that upon viral binding, ACE2 catalytic activity could be inhibited; therefore, impacting the regulation of the renin-angiotensin-aldosterone system (RAAS). To date, only few studies have evaluated the impact of SARS-CoV-2 infection on the blood levels of the components of the RAAS. The objective of this study was to determine the blood levels of ACE, ACE2, angiotensin-II, angiotensin (1-7), and angiotensin (1-9) at hospital admission and discharge in a group of patients presenting with severe or critical evolution of coronavirus disease 2019 (COVID-19). We showed that ACE, ACE2, angiotensin (1-7), and angiotensin (1-9) were similar in patients with critical and severe COVID-19. However, at admission, angiotensin-II levels were significantly higher in patients presenting as critical, compared to patients presenting with severe COVID-19. We conclude that blood levels of angiotensin-II are increased in hospitalized patients with COVID-19 presenting the critical outcome of the disease. We propose that early measurement of Ang-II could be a useful biomarker for identifying patients at higher risk for extremely severe progression of the disease.

摘要

严重急性呼吸综合征冠状病毒2(SARS-CoV-2)利用血管紧张素转换酶2(ACE2)作为其进入细胞的受体,并且研究表明,病毒结合后,ACE2的催化活性可能受到抑制;因此,会影响肾素-血管紧张素-醛固酮系统(RAAS)的调节。迄今为止,仅有少数研究评估了SARS-CoV-2感染对RAAS组分血液水平的影响。本研究的目的是确定一组患有2019冠状病毒病(COVID-19)严重或危重型病情进展的患者入院时和出院时血液中ACE、ACE2、血管紧张素II、血管紧张素(1-7)和血管紧张素(1-9)的水平。我们发现,ACE、ACE2、血管紧张素(1-7)和血管紧张素(1-9)在危重型和重型COVID-19患者中相似。然而,入院时,与重型COVID-19患者相比,危重型患者的血管紧张素II水平显著更高。我们得出结论,患有COVID-19且呈现疾病危重型转归的住院患者血液中血管紧张素II水平升高。我们提出,早期检测血管紧张素II可能是一种有用的生物标志物,用于识别疾病进展为极重型的高风险患者。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03bd/9263116/bbb9c48fc46f/fcvm-09-847809-g001.jpg

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