| Popis: |
The course of COVID-19 in patients is often complicated by hypercoagulation and thrombosis of the great vessels. Vaccination against COVID-19 with ChAdOx1 nCoV-19 (AstraZeneca) in a number of patients turned out to cause thrombocytopenia and thrombi formation in atypical (cerebral venous sinus, portal, abdominal, and hepatic veins) and typical (deep femoral and sural veins, pulmonary artery thromboembolia, acute arterial thrombosis) places. And the use of mRNA vaccines (Moderna and Pfizer) was sometimes accompanied by thrombocytopenia and hemorrhage, but without thrombi formation. This circumstance gave rise to the search for mechanisms of thrombi formation when using previously never-used vaccines developed against COVID-19. The purpose of the paper is to inform the medical community about the mechanisms of thrombi formation in COVID-19; to discuss possible pathogenetic ways of rapid amyloid formation and amyloidogenic stimulation of the coagulation hemostasis system. The only study completed to date provides information on the launch of rapid amyloid formation with the formation of dense large fibrin clots in the whole blood of both healthy people and those who were in the acute period of COVID‑19 disease by the spike protein of the COVID-19 virus capsid. The authors, having discovered the fact of the direct influence of spike protein on the formation of blood clots, nevertheless did not investigate possible pathogenetic ways of triggering thrombi formation by the spike protein. Since the authors directly pointed out the role of rapid amyloid formation in triggering coagulation, the mechanism of which is unknown to practitioners, it makes sense to discuss the issues of rapid amyloid formation in the vascular bed and the role of amyloid as a factor in triggering coagulation hemostasis. The publication under discussion is confirmed by previous studies of other authors on the influence of b‑amyloid and AA‑amyloid on the formation of blood clots in Alzheimer's disease and systemic amyloidosis. Based on the literature sources studied, we suggested that some of the patients who recovered from COVID-19 in its severe form may subsequently develop systemic amyloidosis. |
