Current Practice in Medical Science Vol. 6

Abstract

Background: Thromboembolic complications have been reported as a life-threatening major pathologic event in severe coronavirus disease 2019 (COVID-19) affecting the lung as evidenced by autopsy reports of alveolar damage and pulmonary intravascular microthrombi. The new coronavirus (CoV) does not appear to have intrinsic procoagulant effects itself. The coagulation changes in COVID-19 are likely a result of the inflammatory response. Significant inflammation is present in COVID-19, based on elevated interleukin-6 (IL-6). This inflammation associated with COVID-19 results in coagulopathy, based on elevated D-dimer (DD). An endotheliopathy appears to contribute to microvascular thrombosis in COVID-19. The aim of this study is to confirm the coagulation abnormalities in 100 severe COVID-19 patients having lung involvement and their association with the severity and prognosis.

Method: Inflammation, endothelial and coagulation indicators were performed and compared between severe and mild disease.

Results: IL-6 and TNF-a, and TF and VWF, exceeded in severe COVID-19 patients as well as D-dimer, TAT and Fibrinogen. As PF4 has a rapid removal from plasma, we also measured $\beta$-TG levels which exceeded the plasma levels of PF4 in severe COVID-19 patients as well as increased platelet adhesion was observed. Shortened CT and CFT, high MCF and low LY at 30 minutes were present in 100% of severe COVID-19 patients compared with mild COVID-19 patients.

Conclusions: It is reported that TFPI is a natural anticoagulant that lowers inflammation and coagulation. Therefore, we measured TFPI levels which exceeded without shutdown of the inflammation and coagulation documenting the clinical severity of severe COVID-19 patients.