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The Burden of Hypercoagulability in COVID-19

The novel coronavirus disease 2019 (COVID-19) infection has widespread impact on multiple organ systems, including damage to endothelial cells. Various studies have found evidence for direct mechanisms by which interaction between severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) and endo...

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Autores principales: Kim, Madeleine, George, Andrew, Ganti, Latha, Huang, Derrick, Carman, Matthew
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Georg Thieme Verlag KG 2022
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9054923/
https://www.ncbi.nlm.nih.gov/pubmed/35707624
http://dx.doi.org/10.1055/a-1760-0445
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author Kim, Madeleine
George, Andrew
Ganti, Latha
Huang, Derrick
Carman, Matthew
author_facet Kim, Madeleine
George, Andrew
Ganti, Latha
Huang, Derrick
Carman, Matthew
author_sort Kim, Madeleine
collection PubMed
description The novel coronavirus disease 2019 (COVID-19) infection has widespread impact on multiple organ systems, including damage to endothelial cells. Various studies have found evidence for direct mechanisms by which interaction between severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) and endothelial cells lead to extensive damage to the latter, and indirect mechanisms, such as excessively elevated cytokines, can also result in the same outcome. Damage to the endothelium results in release of thrombotic factors and inhibition of fibrinolysis. This confers a significant hypercoagulability burden on patients infected or recovering from COVID-19 infection. In this case report, the authors report the case of a gentleman presenting with extensive deep vein thrombosis and pulmonary embolism, in the context of recent COVID-19 infection. The postulated mechanisms and management are discussed.
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spelling pubmed-90549232022-06-14 The Burden of Hypercoagulability in COVID-19 Kim, Madeleine George, Andrew Ganti, Latha Huang, Derrick Carman, Matthew TH Open The novel coronavirus disease 2019 (COVID-19) infection has widespread impact on multiple organ systems, including damage to endothelial cells. Various studies have found evidence for direct mechanisms by which interaction between severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) and endothelial cells lead to extensive damage to the latter, and indirect mechanisms, such as excessively elevated cytokines, can also result in the same outcome. Damage to the endothelium results in release of thrombotic factors and inhibition of fibrinolysis. This confers a significant hypercoagulability burden on patients infected or recovering from COVID-19 infection. In this case report, the authors report the case of a gentleman presenting with extensive deep vein thrombosis and pulmonary embolism, in the context of recent COVID-19 infection. The postulated mechanisms and management are discussed. Georg Thieme Verlag KG 2022-02-03 /pmc/articles/PMC9054923/ /pubmed/35707624 http://dx.doi.org/10.1055/a-1760-0445 Text en The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. ( https://creativecommons.org/licenses/by/4.0/ ) https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Kim, Madeleine
George, Andrew
Ganti, Latha
Huang, Derrick
Carman, Matthew
The Burden of Hypercoagulability in COVID-19
title The Burden of Hypercoagulability in COVID-19
title_full The Burden of Hypercoagulability in COVID-19
title_fullStr The Burden of Hypercoagulability in COVID-19
title_full_unstemmed The Burden of Hypercoagulability in COVID-19
title_short The Burden of Hypercoagulability in COVID-19
title_sort burden of hypercoagulability in covid-19
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9054923/
https://www.ncbi.nlm.nih.gov/pubmed/35707624
http://dx.doi.org/10.1055/a-1760-0445
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