COVID-19 and immunothrombosis: Pathophysiology and therapeutic implications.
Crit Rev Oncol Hematol
; 168: 103529, 2021 Dec.
Article
en En
| MEDLINE
| ID: mdl-34800652
ABSTRACT
The coagulopathy of COVID-19 is characterised by significantly elevated D Dimer and fibrinogen, mild thrombocytopenia and a mildly prolonged PT/APTT. A high incidence of thrombotic complications occurs despite standard thromboprophylaxis. The evidence to date supports immunothrombosis as the underlying mechanism for this coagulopathy which is triggered by a hyperinflammatory response and endotheliopathy. A hypercoagulable state results from endothelial damage/activation, complement activation, platelet hyperactivity, release of Extracellular Neutrophil Traps, activation of the coagulation system and a "hypofibrinolytic" state. Significant cross-talk occurs between the innate/adaptive immune system, endothelium and the coagulation system. D dimer has been shown to be the most reliable predictor of disease severity, thrombosis, and overall survival. In this context, targeting pathways upstream of coagulation using novel or repurposed drugs alone or in combination with other anti-thrombotic agents may be a rational approach to prevent the mortality/morbidity due to COVID-19 associated coagulopathy.
Palabras clave
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Tromboembolia Venosa
/
COVID-19
Límite:
Humans
Idioma:
En
Revista:
Crit Rev Oncol Hematol
Asunto de la revista:
HEMATOLOGIA
/
NEOPLASIAS
Año:
2021
Tipo del documento:
Article