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10.1530/EJE-20-1445

http://scihub22266oqcxt.onion/10.1530/EJE-20-1445
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33539316!9494311!33539316
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suck abstract from ncbi


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pmid33539316      Eur+J+Endocrinol 2021 ; 184 (4): 543-552
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  • Renin-angiotensin-aldosterone system peptide profiles in patients with COVID-19 #MMPMID33539316
  • Kutz A; Conen A; Gregoriano C; Haubitz S; Koch D; Domenig O; Bernasconi L; Mueller B; Schuetz P
  • Eur J Endocrinol 2021[Apr]; 184 (4): 543-552 PMID33539316show ga
  • OBJECTIVE: While evidence on the interface between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and the renin-angiotensin-aldosterone-system (RAAS) is accumulating, clinical data on RAAS peptide alteration among coronavirus disease-19 (COVID-19) patients is missing. DESIGN AND METHODS: In this exploratory study, we prospectively included adult patients (aged >/= 18 years) admitted between February 26 and April 30, 2020 to a tertiary care hospital in Switzerland. We assessed the association of an underlying SARS-CoV-2 infection and equilibrium serum levels of RAAS peptides in hospitalized COVID-19 patients 1:1 propensity-score matched with patients suffering from SARS-CoV-2-negative respiratory infections. Subgroup analyses involved stratification for taking RAAS inhibitors. RESULTS: COVID-19 patients had about 50% lower equilibrium serum RAAS peptide levels as compared with matched controls (angiotensin I: 31.6 vs 66.8 pmol/L, -52.7% (95%CI: -68.5% to -36.9%); angiotensin II: 37.7 vs 92.5 pmol/L, -59.2% (95%CI: -72.1% to -46.3%); angiotensin (1-5): 3.3 vs 6.6 pmol/L, -49.7% (95%CI: -59.2% to -40.2%); angiotensin (1-7): 4.8 vs 7.6 pmol/L, -64.9% (95%CI: -84.5% to -45.3%)). While the plasma renin activity was lower in COVID-19 patients (88.6 vs 207.9 pmol/L, -58.5% (95%CI: -71.4% to -45.6%)), there was no difference of angiotensin-converting enzyme (ACE) and ACE2 plasma activity between the groups. Subgroup analyses revealed a pronounced RAAS peptide profile depression in COVID-19 patients among those not on RAAS inhibitors. CONCLUSIONS: As compared with SARS-CoV-2-negative patients, we found a downregulated RAAS in presence of a SARS-CoV-2 infection. Whether the lower levels of the protective angiotensin (1-5) and (1-7) are linked to adverse outcomes in COVID-19 warrants further investigation.
  • |Adrenergic beta-Antagonists/therapeutic use[MESH]
  • |Aged[MESH]
  • |Angiotensin I/*blood[MESH]
  • |Angiotensin II/*blood[MESH]
  • |Angiotensin Receptor Antagonists/therapeutic use[MESH]
  • |Angiotensin-Converting Enzyme 2/*blood[MESH]
  • |Angiotensin-Converting Enzyme Inhibitors/therapeutic use[MESH]
  • |COVID-19/*blood[MESH]
  • |Case-Control Studies[MESH]
  • |Female[MESH]
  • |Humans[MESH]
  • |Male[MESH]
  • |Middle Aged[MESH]
  • |Peptide Fragments/*blood[MESH]
  • |Peptidyl-Dipeptidase A/*blood[MESH]
  • |Prospective Studies[MESH]
  • |Renin-Angiotensin System[MESH]
  • |Renin/*blood[MESH]


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