Genetic triggers prothrombogenic status in Covid-19

ABSTRACT

Background: Currently, the prothrombogenic status in Covid-19 infection and the possible influence of genetic polymorphism of the hemostasis system are widely discussed. Aim(s) The aim of the study was to evaluate the molecular and genetic features of the hemostasis system in patients with Covid-19 Methods: The study was performed on the basis of the regional center for antithrombotic therapy Arkhangelsk.A molecular genetic analysis was performed for the presence of prothrombogenic mutations in patients (n = 100) with Covid-19 in a covid hospital. Result(s) Polymorphism in the F I G/A-455 (fibrinogen) gene was found in 43% of patients (homozygote -6%, heterozygote -37%), polymorphism in the ITG B3 1565 T>C gene -in 38% (26% -heterozygous carrier and 12% -homozygous). In our study, a mutation in the prothrombin F II gene G20210-A (heterozygous allelic variant -2%) and a "true" prothrombogenic mutation of factor V (Leid) were found with the lowest (6% -heterozygous state). Next, we analyzed the dependence of genetic polymorphism of hemostasis system factors F II 20210 G>A, F V 1691 G>A, PAI-1 675 5G>4G and thrombinemia levels in patients with COVID-19. The level of fibrinogen (>6.0 g/l;p < 0.05) was statistically significantly higher in the groups of patients with prothrombogenic polymorphism in the genes of coagulation factor V (F V), coagulation factor II (F II), PAI-1 for the entire period of hospitalization. Upon admission, the levels of D-dimer and fibrinogen were statistically significantly higher in patients with a mutation in the F II gene. Conclusion(s) When treating Covid-19, it is advisable to take into account the presence of molecular genetic markers of prothrombogenic status in a patient.