Abstract
The aim of the work. To investigate platelet aggregation, polymorphism in the genes that ensure its implementation, and the association between these indicators in patients with COVID-19-associated lung damage, depending on the severity of the clinical course. Methodology. The study involved 75 patients with COVID-19, which, depending on the severity of lung involvement, were divided into two groups: patients with damage of up to 50 % of the lung parenchyma (n = 48) and with damage of more than 50 % (n = 27) respectively. The control group consisted of healthy people (n = 24), comparable in sex and age. In all individuals, the number of platelets, platelet aggregation induced by ADP, collagen and ristomycin were studied; polymorphisms rs6065 in the GP1BA gene, rs1126643 in the ITGA2 gene, and rs5918 in the ITGB3 gene were determined by polymerase chain reaction. The analysis of the obtained data was executed using the IBM SPSS Statistics v. 23 (IMB Corp., USA). Results and discussion. In patients with moderate and severe COVID-19-associated lung damage, platelet aggregation induced by ADP, collagen, and ristomycin accelerated; in severe cases, the number of platelets decreased. The frequency of variants of the rs6065 polymorphism did not change, the frequency of occurrence of the T/C genotype of the rs5918 polymorphism increased; with moderate severity, the frequency of occurrence of the C/T and T/T genotypes of the rs1126643 polymorphism increased; with severe lung damage, the frequency of occurrence of the mutant C/C genotype polymorphism rs5918 increased. In moderate lung damage, the presence of the mutant T/T polymorphism rs1126643 accelerated collagen-induced platelet aggregation; in severe cases, the presence of mutant C/C and heterozygous variant C/T polymorphism rs5918 accelerated ADP-induced platelet aggregation. There was no effect of the rs6065 polymorphism on platelet aggregation. The data obtained indicate the possible role of genetic predisposition in the activation of platelet aggregation in patients with COVID-19-associated lung damage.
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