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COVID-19 and immunothrombosis: Pathophysiology and therapeutic implications
1Department of Hematology, Launceston General Hospital, WP Holman Clinic, Level 1. PO Box 1963, Launceston, Tasmania, Australia.
Critical Reviews in Oncology/Hematology
|November 20, 2021
Summary
COVID-19 coagulopathy involves high D-dimer and fibrinogen, leading to thrombotic events. Targeting upstream pathways may prevent severe outcomes and mortality.
Area of Science:
- Hematology
- Immunology
- Virology
Background:
- COVID-19 coagulopathy presents with elevated D-dimer and fibrinogen, mild thrombocytopenia, and prolonged PT/APTT.
- High rates of thrombosis occur despite standard prophylaxis, suggesting underlying mechanisms beyond simple hypercoagulation.
Purpose of the Study:
- To elucidate the immunothrombosis mechanism in COVID-19.
- To identify reliable predictors of disease severity and thrombosis.
- To explore rational therapeutic strategies targeting upstream pathways.
Main Methods:
- Review of current evidence on COVID-19 coagulopathy.
- Analysis of biomarkers such as D-dimer.
- Examination of the interplay between immune response, endothelium, and coagulation.
Main Results:
- Immunothrombosis, driven by hyperinflammation and endotheliopathy, underlies COVID-19 coagulopathy.
- Endothelial damage, complement activation, platelet hyperactivity, NETs, and hypofibrinolysis contribute to a hypercoagulable state.
- Elevated D-dimer is the most reliable predictor of disease severity, thrombosis, and survival.
Conclusions:
- Targeting upstream coagulation pathways with novel or repurposed drugs is a rational approach.
- Combination therapies may enhance prevention of mortality and morbidity associated with COVID-19 coagulopathy.
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