tetano
Editor, Senior Moderator
Med Arch
. 2022 Feb;76(1):62-65.
doi: 10.5455/medarh.2022.76.62-65.
Multi-factorial Mechanism Behind COVID-19 Related Thrombosis
Elshazali Widaa Ali[SUP] 1 2 [/SUP], Ibrahim Khedir Ibrahim[SUP] 2 [/SUP]
Affiliations
Abstract
Background: Thrombosis plays a crucial role in the morbidity and mortality of coronavirus disease-19 (COVID-19). About one-third of COVID-19 patients experience a thrombotic event, most commonly pulmonary embolism. Based on published data, the mechanism of thrombosis in COVID-19 patients seems to be multi-factorial.
Methods: In this article, we reviewed the publsihed data concerning with thrombosis in COVID-19 and summarized the predisposing factors and the mechanisms behind COVID-19 related thrombosis.
Results: Inflammatory response to SARS-CoV-2 and the consequent hyperviscosity thought to cause endothelial damage and initiate coagulation. Furthermore, inflammation promotes platelet activation and exerts a pathogenic effect on endothelial cells. The presence of anticardiolipin and anti-β2-glycoprotein antibodies in some patients with COVID-19 suggests that SARS-CoV-2, like many other viral infections, induces the formation of antiphospholipid antibodies, which provoke hypercoagulability. Thrombophilic mutations, mainly factor V Leiden and prothrombin G20201A mutations, can be a contributing factor in the development of thrombosis in COVID-19 patients, and they are associated with increased disease severity and pulmonary embolism. However, the research concerning with the association of thrombophilic mutations with COVID-19 related thrombosis showed conflict results.
Conclusion: The mechanism of thrombosis in COVID-19 patients seems to be multifactorial. Endothelial damage, antiphospholipid antibodies, inflammation, hyperviscosity, and thrombophilic mutations are the main factors that predispose COVID-19 patients to. thrombosis.
Keywords: Antiphospholipid antibodies; COVID-19; Hyperviscosity; Inflammation; Thrombosis; thrombophilia.
. 2022 Feb;76(1):62-65.
doi: 10.5455/medarh.2022.76.62-65.
Multi-factorial Mechanism Behind COVID-19 Related Thrombosis
Elshazali Widaa Ali[SUP] 1 2 [/SUP], Ibrahim Khedir Ibrahim[SUP] 2 [/SUP]
Affiliations
- PMID: 35422572
- PMCID: PMC8976895
- DOI: 10.5455/medarh.2022.76.62-65
Abstract
Background: Thrombosis plays a crucial role in the morbidity and mortality of coronavirus disease-19 (COVID-19). About one-third of COVID-19 patients experience a thrombotic event, most commonly pulmonary embolism. Based on published data, the mechanism of thrombosis in COVID-19 patients seems to be multi-factorial.
Methods: In this article, we reviewed the publsihed data concerning with thrombosis in COVID-19 and summarized the predisposing factors and the mechanisms behind COVID-19 related thrombosis.
Results: Inflammatory response to SARS-CoV-2 and the consequent hyperviscosity thought to cause endothelial damage and initiate coagulation. Furthermore, inflammation promotes platelet activation and exerts a pathogenic effect on endothelial cells. The presence of anticardiolipin and anti-β2-glycoprotein antibodies in some patients with COVID-19 suggests that SARS-CoV-2, like many other viral infections, induces the formation of antiphospholipid antibodies, which provoke hypercoagulability. Thrombophilic mutations, mainly factor V Leiden and prothrombin G20201A mutations, can be a contributing factor in the development of thrombosis in COVID-19 patients, and they are associated with increased disease severity and pulmonary embolism. However, the research concerning with the association of thrombophilic mutations with COVID-19 related thrombosis showed conflict results.
Conclusion: The mechanism of thrombosis in COVID-19 patients seems to be multifactorial. Endothelial damage, antiphospholipid antibodies, inflammation, hyperviscosity, and thrombophilic mutations are the main factors that predispose COVID-19 patients to. thrombosis.
Keywords: Antiphospholipid antibodies; COVID-19; Hyperviscosity; Inflammation; Thrombosis; thrombophilia.