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Published on: September 9, 2012
Multi-factorial Mechanism Behind COVID-19 Related Thrombosis
Elshazali Widaa Ali1,2, Ibrahim Khedir Ibrahim2
1Department of Medical Laboratory Sciences, College of Applied Medical Science, University of Bisha, Bisha, Saudi Arabia.
Insights
COVID-19 patients face a high risk of thrombosis due to multifactorial causes. Key factors include inflammation, endothelial damage, and antiphospholipid antibodies, contributing to severe outcomes like pulmonary embolism.
Area of Science:
- Medical Science
- Virology
- Hematology
Background:
- Thrombosis is a significant complication of COVID-19, affecting approximately one-third of patients.
- Pulmonary embolism is the most common thrombotic event observed in COVID-19 cases.
Purpose of the Study:
- To review published data on COVID-19 related thrombosis.
- To summarize predisposing factors and mechanisms of thrombosis in COVID-19.
Main Methods:
- Systematic review of existing literature on COVID-19 and thrombosis.
- Analysis of predisposing factors and etiological mechanisms.
Main Results:
- COVID-19 thrombosis is multifactorial, involving inflammation, hyperviscosity, and endothelial damage.
- SARS-CoV-2 infection can induce antiphospholipid antibodies, increasing hypercoagulability.
- Thrombophilic mutations (e.g., Factor V Leiden) may contribute to thrombosis and disease severity, though research is conflicting.
Conclusions:
- The multifactorial nature of COVID-19 thrombosis involves endothelial damage, antiphospholipid antibodies, inflammation, hyperviscosity, and thrombophilic mutations.
- These factors collectively predispose COVID-19 patients to thrombotic events.
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.
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