“…127,128 Similar results were highlighted during the 2003 SARS-CoVepidemic. 129,130 Today, significantly increased PAI-1 values have been found in multiple studies on patients with COVID-19, with some studies reporting values up to fourfold higher in COVID-19 patients compared with control groups. 123,131 This overload of PAI-1 in SARS-CoV-2 infection can be further aggravated by raised angiotensin II levels in the blood of patients with COVID-19, with PAI-1 levels being upregulated in the endothelial cells, resulting in elevated circulatory PAI-1 levels.…”
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.
“…127,128 Similar results were highlighted during the 2003 SARS-CoVepidemic. 129,130 Today, significantly increased PAI-1 values have been found in multiple studies on patients with COVID-19, with some studies reporting values up to fourfold higher in COVID-19 patients compared with control groups. 123,131 This overload of PAI-1 in SARS-CoV-2 infection can be further aggravated by raised angiotensin II levels in the blood of patients with COVID-19, with PAI-1 levels being upregulated in the endothelial cells, resulting in elevated circulatory PAI-1 levels.…”
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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