Journal
SEMINARS IN THROMBOSIS AND HEMOSTASIS
Volume 48, Issue 1, Pages 19-30Publisher
THIEME MEDICAL PUBL INC
DOI: 10.1055/s-0041-1736166
Keywords
SARS-CoV-2; COVID-19; coagulopathy; thrombosis
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The main pathology of COVID-19 involves infection of pulmonary tract cells, leading to an inflammatory response and coagulation disorders that can result in thrombotic events. Understanding the pathophysiological mechanisms behind these events is crucial for developing more effective therapeutic strategies.
The cardinal pathology of coronavirus disease 2019 (COVID-19) is a primary infection of pulmonary tract cells by severe acute respiratory syndrome coronavirus 2, provoking a local inflammatory response, often accompanied by cytokine storm and acute respiratory distress syndrome, especially in patients with severe disease. Systemic propagation of the disease may associate with thrombotic events, including deep vein thrombosis, pulmonary embolism, and thrombotic microangiopathy, which are important causes of morbidity and mortality in patients with COVID-19. This narrative review describes current knowledge of the pathophysiological mechanisms of COVID-19-associated coagulopathy, with focus on prothrombotic changes in hemostatic mediators, including plasma levels of clotting factors, natural anticoagulants, components of fibrinolytic system, and platelets. It will also highlight the central role of endothelial cells in COVID-19-associated coagulopathy. This narrative review discusses also potential therapeutic strategies for managing thrombotic complications. Awareness by medical experts of contributors to the pathogenesis of thrombotic events in COVID-19 is imperative to develop therapeutics not limited to regular anticoagulants. Instituting cooperation among medical personnel and researchers may lessen this novel virus' impact now, and in the event of recurrence.
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