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dc.contributor.authorHanff, Thomas C. et al.
dc.date.accessioned2020-05-05T14:37:45Z
dc.date.available2020-05-05T14:37:45Z
dc.date.issued2020-03-26
dc.identifier.urihttps://doi.org/10.1093/cid/ciaa329en_US
dc.identifier.urihttps://hdl.handle.net/20.500.12663/1307
dc.description.abstractMortality from coronavirus disease 2019 (COVID-19) is strongly associated with cardiovascular disease, diabetes, and hypertension. These disorders share underlying pathophysiology related to the renin-angiotensin system (RAS) that may be clinically insightful. In particular, activity of the angiotensin-converting enzyme 2 (ACE2) is dysregulated in cardiovascular disease, and this enzyme is used by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to initiate the infection. Cardiovascular disease and pharmacologic RAS inhibition both increase ACE2 levels, which may increase the virulence of SARS-CoV-2 within the lung and heart. Conversely, mechanistic evidence from related coronaviruses suggests that SARS-CoV-2 infection may downregulate ACE2, leading to toxic overaccumulation of Angiotensin II that induces acute respiratory distress syndrome and fulminant myocarditis. RAS inhibition could mitigate this effect. With conflicting mechanistic evidence, we propose key clinical research priorities necessary to clarify the role of RAS inhibition in COVID-19 mortality that could be rapidly addressed by the international research community.en_US
dc.languageEnglishen_US
dc.subjectCOVID-19en_US
dc.subjectCoronavirusen_US
dc.subjectInfectious Diseasesen_US
dc.subjectEpidemiologyen_US
dc.subjectRenin-Angiotensin Systemen_US
dc.titleIs There an Association Between COVID-19 Mortality and the Renin-Angiotensin System—a Call for Epidemiologic Investigationsen_US
eihealth.countryOthersen_US
eihealth.categoryClinical characterization and managementen_US
eihealth.typePublished Articleen_US
eihealth.maincategorySave Lives / Salvar Vidasen_US
dc.relation.ispartofjournalClinical Infectious Diseasesen_US


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