Does COVID-19-related viral sepsis stimulate angiotensin II levels more than bacterial sepsis?

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dc.authoridbicakcioglu, murat/0000-0001-9101-6857
dc.authorwosidbicakcioglu, murat/AAA-8149-2022
dc.contributor.authorDemircan, Selcuk
dc.contributor.authorBulut, Niluefer
dc.contributor.authorKalkan, Serkan
dc.contributor.authorDuzenci, Deccane
dc.contributor.authorBicakcioglu, Murat
dc.contributor.authorOzden, Mehmet
dc.contributor.authorDogan, Zafer
dc.date.accessioned2024-08-04T20:57:42Z
dc.date.available2024-08-04T20:57:42Z
dc.date.issued2023
dc.departmentİnönü Üniversitesien_US
dc.description.abstractAim: Angiotensin II and its receptors play a role in both COVID and bacterial sepsis. The aim of this study was to compare the levels of serum angiotensin II and its receptors in viral sepsis due to COVID-19 with the levels in bacterial sepsis.Material and Methods: The study included 62 sepsis patients (n=31 COVID and n=31 non-COVID) with similar disease severity in the tertiary ICU. The serum angiotensin II, angiotensin II receptors 1 and 2 (ATR1, ATR2) and other inflammatory parameters were measured. Demographic data and 28-day mortality were recorded.Results: Angiotensin II level was significantly higher in COVID patients than in non-COVID patients (p<0.05). ATR1 and ATR2 did not differ between the two groups. There was a negative correlation between angiotensin II and procalcitonin levels in all patients, and a positive correlation between ATR1 and procalcitonin, APACHE II score, and SOFA score in COVID patients (p<0.05).Discussion: Observation showed that angiotensin II levels were higher in patients with COVID-19 compared to those with bacterial sepsis, and ATR1 level was higher in COVID-19 patients who died. It was thought that the renin-angiotensin cascade could be stimulated differently in bacterial sepsis compared to viral sepsis due to COVID.en_US
dc.identifier.doi10.4328/ACAM.21713
dc.identifier.endpage720en_US
dc.identifier.issn2667-663X
dc.identifier.issue8en_US
dc.identifier.startpage716en_US
dc.identifier.urihttps://doi.org/10.4328/ACAM.21713
dc.identifier.urihttps://hdl.handle.net/11616/102857
dc.identifier.volume14en_US
dc.identifier.wosWOS:001050540900011en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.language.isoenen_US
dc.publisherBayrakol Medical Publisheren_US
dc.relation.ispartofAnnals of Clinical and Analytical Medicineen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectAngiotensin IIen_US
dc.subjectBacterial Infectionen_US
dc.subjectCOVID-19en_US
dc.subjectSepsisen_US
dc.titleDoes COVID-19-related viral sepsis stimulate angiotensin II levels more than bacterial sepsis?en_US
dc.typeArticleen_US

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