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dc.contributor.authorKatneni, Upendra K
dc.contributor.authorAlexaki, Aikaterini
dc.contributor.authorHunt, Ryan C
dc.contributor.authorSchiller, Tal
dc.contributor.authorDiCuccio, Michael
dc.contributor.authorBuehler, Paul W
dc.contributor.authorIbla, Juan C
dc.contributor.authorKimchi-Sarfaty, Chava
dc.date.accessioned2020-09-16T13:46:07Z
dc.date.available2020-09-16T13:46:07Z
dc.date.issued2020-08-24
dc.identifier.urihttp://hdl.handle.net/10713/13711
dc.description.abstractCoronavirus disease of 2019 (COVID-19) is the clinical manifestation of the respiratory infection caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). While primarily recognized as a respiratory disease, it is clear that COVID-19 is systemic illness impacting multiple organ systems. One defining clinical feature of COVID-19 has been the high incidence of thrombotic events. The underlying processes and risk factors for the occurrence of thrombotic events in COVID-19 remain inadequately understood. While severe bacterial, viral, or fungal infections are well recognized to activate the coagulation system, COVID-19-associated coagulopathy is likely to have unique mechanistic features. Inflammatory-driven processes are likely primary drivers of coagulopathy in COVID-19, but the exact mechanisms linking inflammation to dysregulated hemostasis and thrombosis are yet to be delineated. Cumulative findings of microvascular thrombosis has raised question if the endothelium and microvasculature should be a point of investigative focus. von Willebrand factor (VWF) and its protease, a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS-13), play important role in the maintenance of microvascular hemostasis. In inflammatory conditions, imbalanced VWF-ADAMTS-13 characterized by elevated VWF levels and inhibited and/or reduced activity of ADAMTS-13 has been reported. Also, an imbalance between ADAMTS-13 activity and VWF antigen is associated with organ dysfunction and death in patients with systemic inflammation. A thorough understanding of VWF-ADAMTS-13 interactions during early and advanced phases of COVID-19 could help better define the pathophysiology, guide thromboprophylaxis and treatment, and improve clinical prognosis.en_US
dc.description.urihttps://doi.org/10.1055/s-0040-1715841en_US
dc.language.isoenen_US
dc.publisherThiemeen_US
dc.relation.ispartofThrombosis and Haemostasisen_US
dc.rightsThieme. All rights reserved.en_US
dc.subjectCOVID-19en_US
dc.subjectthrombosisen_US
dc.subjectinflammationen_US
dc.subjectADAMTS-13en_US
dc.subjectvon Willebrand factoren_US
dc.titleCoagulopathy and Thrombosis as a Result of Severe COVID-19 Infection: A Microvascular Focusen_US
dc.typeArticleen_US
dc.identifier.doi10.1055/s-0040-1715841
dc.identifier.pmid32838472
dc.source.countryGermany


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