COVID-19 coagulopathy, thrombosis, and bleeding

Abstract

In this issue of Blood, Al-Samkari et al expand our understanding of thrombosis and bleeding risks and their predictors in hospitalized patients with coronavirus disease 2019 (COVID-19).

Potential mechanism linking dysregulated inflammation and coagulation with thrombosis. SARS-CoV-2 infects respiratory epithelial cells by binding to the angiotensin-converting enzyme 2 (ACE-2) receptor. Shed virus elicits an inflammatory response, which can be maladaptive in some cases leading to a cytokine storm mediated by proinflammatory cytokines such as interleukin 1β (IL-1β), IL-2, IL-6, tumor necrosis factor (TNF), and granulocyte-macrophage colony-stimulating factor (GM-CSF). Proinflammatory cytokines and SARS-CoV-2 infection of the endothelium contribute to hypercoagulability by upregulation of procoagulants such as tissue factor (TF), P-selectin, factor VIII (FVIII), fibrinogen, and von Willebrand factor (vWF); downregulation of anticoagulants such as thrombomodulin (TM) and endothelial protein C receptor (EPCR); and modulation of fibrinolysis by increased expression of type 1 plasminogen activator inhibitor, and leukocyte recruitment. Finally, the hypoxia and immobility in hospitalized patients with COVID-19 are potent triggers of thrombosis. Illustration created with BioRender.com.