Magda Rurua, Elena Pachkoria, Tamar Sanikidze, K Machvariani, George Ormocadze, Tinatin Jomidava, Diana Dzidziguri, Levan Ratiani
{"title":"血管紧张素转换酶(ACE)抑制剂对COVID-19和其他严重呼吸道感染在高铁素血症条件下发生的急性呼吸窘迫综合征(ARDS)病程的影响:一项队列研究","authors":"Magda Rurua, Elena Pachkoria, Tamar Sanikidze, K Machvariani, George Ormocadze, Tinatin Jomidava, Diana Dzidziguri, Levan Ratiani","doi":"10.1177/11795484231180391","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Angiotensin-converting enzyme 2 (ACE2) is not only the entry route of SARS-CoV-2 infection but also triggers a major mechanism of COVID-19 aggravation by promoting a hyperinflammatory state, leading to lung injury, hematological and immunological dysregulation. The impact of ACE2 inhibitors on the course of COVID-19 is still unclear. The effect of ACE2 inhibitors on the course of acute respiratory distress syndrome (ARDS) during COVID-19 and other severe respiratory infections in conditions of hyperferritinemia (HF) was investigated.</p><p><strong>Methods: </strong>A cohort study of critically ill patients with COVID-19 and other respiratory diseases (widespread infection, pneumonia) who underwent treatment in The Critical Care Unit of the First University Clinic (Tbilisi, Georgia) during the 2020-2021 years was conducted. The impact of the ACE2 inhibitors on the course of the ARDS developed during COVID-19 and other severe respiratory infections in conditions of different severity of HF was evaluated.</p><p><strong>Results: </strong>In COVID-19-infected (I) and uninfected (II) patients with ARDS, ACE2 inhibitors reduce the levels of Ang II, C reactive protein (CRP) and D-dimer (I: from 1508.07 ± 26.68 to 48.51 ± 24.35, from 233.92 ± 13.02 to 198.12 ± 11.88, from 7.88 ± 0.47 to 6.28 ± 0.43; II: from 1000.14 ± 149.49 to 46.23 ± 88.21, 226.48 ± 13.81 to 183.52 ± 17.32, from 6.39 ± 0.58 to 5.48 ± 0.69) at moderate HF and Ang II, CRP levels (I: from 1845.89 ± 89.37 to 49.64 ± 51.05, from 209.28 ± 14.41 to 175.37 ± 9.84; II: from 1753.29 ± 65.95 to 49.76 ± 55.74, 287.10 ± 20.50 to 214.71 ± 17.32) at severe HF, reduce interleukin-6 (IL-6) expression at moderate HF (I: from 1977.23 ± 354.66 to 899.36 ± 323.76) and cause reduction of pCO<sub>2</sub> index at severe HF (I: from 69.80 ± 3.22 to 60.44 ± 2.20) in COVID-19-infected patients.</p><p><strong>Conclusion: </strong>Study results show that the ACE2 inhibitors play an important role in the regulation of inflammatory processes in both COVID-19-infected and uninfected patients with ARDS. ACE2 inhibitors decrease immunological disorders, inflammation, and lung alveoli dysfunction, especially in COVID-19-infected patients.</p>","PeriodicalId":1,"journal":{"name":"Accounts of Chemical Research","volume":null,"pages":null},"PeriodicalIF":16.4000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/4f/9f/10.1177_11795484231180391.PMC10259131.pdf","citationCount":"0","resultStr":"{\"title\":\"Impact of the Angiotensin-Converting Enzyme (ACE) Inhibitors on the Course of the Acute Respiratory Distress Syndrome (ARDS) Developed During COVID-19 and Other Severe Respiratory Infections Under Hyperferritinemia Conditions: A Cohort Study.\",\"authors\":\"Magda Rurua, Elena Pachkoria, Tamar Sanikidze, K Machvariani, George Ormocadze, Tinatin Jomidava, Diana Dzidziguri, Levan Ratiani\",\"doi\":\"10.1177/11795484231180391\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Angiotensin-converting enzyme 2 (ACE2) is not only the entry route of SARS-CoV-2 infection but also triggers a major mechanism of COVID-19 aggravation by promoting a hyperinflammatory state, leading to lung injury, hematological and immunological dysregulation. The impact of ACE2 inhibitors on the course of COVID-19 is still unclear. The effect of ACE2 inhibitors on the course of acute respiratory distress syndrome (ARDS) during COVID-19 and other severe respiratory infections in conditions of hyperferritinemia (HF) was investigated.</p><p><strong>Methods: </strong>A cohort study of critically ill patients with COVID-19 and other respiratory diseases (widespread infection, pneumonia) who underwent treatment in The Critical Care Unit of the First University Clinic (Tbilisi, Georgia) during the 2020-2021 years was conducted. The impact of the ACE2 inhibitors on the course of the ARDS developed during COVID-19 and other severe respiratory infections in conditions of different severity of HF was evaluated.</p><p><strong>Results: </strong>In COVID-19-infected (I) and uninfected (II) patients with ARDS, ACE2 inhibitors reduce the levels of Ang II, C reactive protein (CRP) and D-dimer (I: from 1508.07 ± 26.68 to 48.51 ± 24.35, from 233.92 ± 13.02 to 198.12 ± 11.88, from 7.88 ± 0.47 to 6.28 ± 0.43; II: from 1000.14 ± 149.49 to 46.23 ± 88.21, 226.48 ± 13.81 to 183.52 ± 17.32, from 6.39 ± 0.58 to 5.48 ± 0.69) at moderate HF and Ang II, CRP levels (I: from 1845.89 ± 89.37 to 49.64 ± 51.05, from 209.28 ± 14.41 to 175.37 ± 9.84; II: from 1753.29 ± 65.95 to 49.76 ± 55.74, 287.10 ± 20.50 to 214.71 ± 17.32) at severe HF, reduce interleukin-6 (IL-6) expression at moderate HF (I: from 1977.23 ± 354.66 to 899.36 ± 323.76) and cause reduction of pCO<sub>2</sub> index at severe HF (I: from 69.80 ± 3.22 to 60.44 ± 2.20) in COVID-19-infected patients.</p><p><strong>Conclusion: </strong>Study results show that the ACE2 inhibitors play an important role in the regulation of inflammatory processes in both COVID-19-infected and uninfected patients with ARDS. ACE2 inhibitors decrease immunological disorders, inflammation, and lung alveoli dysfunction, especially in COVID-19-infected patients.</p>\",\"PeriodicalId\":1,\"journal\":{\"name\":\"Accounts of Chemical Research\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":16.4000,\"publicationDate\":\"2023-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/4f/9f/10.1177_11795484231180391.PMC10259131.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Accounts of Chemical Research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1177/11795484231180391\",\"RegionNum\":1,\"RegionCategory\":\"化学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CHEMISTRY, MULTIDISCIPLINARY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Accounts of Chemical Research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1177/11795484231180391","RegionNum":1,"RegionCategory":"化学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CHEMISTRY, MULTIDISCIPLINARY","Score":null,"Total":0}
Impact of the Angiotensin-Converting Enzyme (ACE) Inhibitors on the Course of the Acute Respiratory Distress Syndrome (ARDS) Developed During COVID-19 and Other Severe Respiratory Infections Under Hyperferritinemia Conditions: A Cohort Study.
Background: Angiotensin-converting enzyme 2 (ACE2) is not only the entry route of SARS-CoV-2 infection but also triggers a major mechanism of COVID-19 aggravation by promoting a hyperinflammatory state, leading to lung injury, hematological and immunological dysregulation. The impact of ACE2 inhibitors on the course of COVID-19 is still unclear. The effect of ACE2 inhibitors on the course of acute respiratory distress syndrome (ARDS) during COVID-19 and other severe respiratory infections in conditions of hyperferritinemia (HF) was investigated.
Methods: A cohort study of critically ill patients with COVID-19 and other respiratory diseases (widespread infection, pneumonia) who underwent treatment in The Critical Care Unit of the First University Clinic (Tbilisi, Georgia) during the 2020-2021 years was conducted. The impact of the ACE2 inhibitors on the course of the ARDS developed during COVID-19 and other severe respiratory infections in conditions of different severity of HF was evaluated.
Results: In COVID-19-infected (I) and uninfected (II) patients with ARDS, ACE2 inhibitors reduce the levels of Ang II, C reactive protein (CRP) and D-dimer (I: from 1508.07 ± 26.68 to 48.51 ± 24.35, from 233.92 ± 13.02 to 198.12 ± 11.88, from 7.88 ± 0.47 to 6.28 ± 0.43; II: from 1000.14 ± 149.49 to 46.23 ± 88.21, 226.48 ± 13.81 to 183.52 ± 17.32, from 6.39 ± 0.58 to 5.48 ± 0.69) at moderate HF and Ang II, CRP levels (I: from 1845.89 ± 89.37 to 49.64 ± 51.05, from 209.28 ± 14.41 to 175.37 ± 9.84; II: from 1753.29 ± 65.95 to 49.76 ± 55.74, 287.10 ± 20.50 to 214.71 ± 17.32) at severe HF, reduce interleukin-6 (IL-6) expression at moderate HF (I: from 1977.23 ± 354.66 to 899.36 ± 323.76) and cause reduction of pCO2 index at severe HF (I: from 69.80 ± 3.22 to 60.44 ± 2.20) in COVID-19-infected patients.
Conclusion: Study results show that the ACE2 inhibitors play an important role in the regulation of inflammatory processes in both COVID-19-infected and uninfected patients with ARDS. ACE2 inhibitors decrease immunological disorders, inflammation, and lung alveoli dysfunction, especially in COVID-19-infected patients.
期刊介绍：
Accounts of Chemical Research presents short, concise and critical articles offering easy-to-read overviews of basic research and applications in all areas of chemistry and biochemistry. These short reviews focus on research from the author’s own laboratory and are designed to teach the reader about a research project. In addition, Accounts of Chemical Research publishes commentaries that give an informed opinion on a current research problem. Special Issues online are devoted to a single topic of unusual activity and significance.
Accounts of Chemical Research replaces the traditional article abstract with an article "Conspectus." These entries synopsize the research affording the reader a closer look at the content and significance of an article. Through this provision of a more detailed description of the article contents, the Conspectus enhances the article's discoverability by search engines and the exposure for the research.
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
