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dc.contributor.authorKolberg, Espen Skarstein
dc.contributor.authorTonby, Kristian
dc.contributor.authorWickstrøm, Kristin
dc.contributor.authorRiise, Anne Margarita Dyrhol
dc.contributor.authorHolten, Aleksander Rygh
dc.contributor.authorAmundsen, Erik Koldberg
dc.date.accessioned2021-01-04T14:31:27Z
dc.date.available2021-01-04T14:31:27Z
dc.date.created2020-12-30T14:10:36Z
dc.date.issued2020
dc.identifier.issn0903-4641
dc.identifier.urihttps://hdl.handle.net/11250/2721321
dc.description.abstractWe have earlier proposed that serum ACE (s‐ACE) could be used as a biomarker for severity in COVID‐19 due to an assumed inverse relationship between ACE and ACE2. High s‐ACE could indicate lower ACE2 activity and therefore more widespread and severe SARS‐CoV2 infection, owing to virally mediated downregulation of ACE2 (1). Dysregulation of the Renin‐Angiotensin‐Aldosterone system (RAAS) are found in comorbidities known as risk factors for increased morbidity and mortality, such as hypertension and cardiovascular disease (2).en_US
dc.language.isoengen_US
dc.publisherWiley Online Libraryen_US
dc.titleSerum ACE as a prognostic biomarker in COVID-19: A Case seriesen_US
dc.typePeer revieweden_US
dc.typeJournal articleen_US
dc.description.versionacceptedVersionen_US
dc.source.journalActa Pathologica, Microbiologica et Immunologica Scandinavica (APMIS)en_US
dc.identifier.doi10.1111/apm.13108
dc.identifier.cristin1864100
dc.description.localcodeFirst published: 23 December 2020.This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi:10.1111/apm.13108en_US
cristin.ispublishedtrue
cristin.fulltextpostprint
cristin.qualitycode1


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