ABSTRACT
Thrombotic and microangiopathic effects have been reported in COVID-19 patients. This study examined the contribution of the hereditary thrombophilia factors Prothrombin (FII) and Factor V Leiden (FVL) genotypes to the severity of COVID-19 disease and the development of thrombosis. This study investigated FII and FVL alleles in a cohort of 9508 patients (2606 male and 6902 female) with thrombophilia. It was observed that 930 of these patients had been infected by SARS-CoV-2 causing COVID-19. The demographic characteristics of the patients and their COVID-19 medical history were recorded. Detailed clinical manifestations were analyzed in a group of cases (n = 4092). This subgroup was age and gender-matched. FII and FVL frequency data of healthy populations without thrombophilia risk were obtained from Bursa Uludag University Medical Genetic Department's Exome Databank. The ratio of males (31.08%; 27.01%) and the mean age (36.85 ± 15.20; 33.89 ± 14.14) were higher among COVID-19 patients compared to non-COVID-19 patients. The prevalence of FVL and computerized tomography (CT) positivity in COVID-19 patients was statistically significant in the thrombotic subgroup (p < 0.05). FVL prevalence, CT positivity rate, history of thrombosis, and pulmonary thromboembolism complication were found to be higher in deceased COVID-19 patients (p < 0.05). Disease severity was mainly affected by FVL and not related to genotypes at the Prothrombin mutations. Overall, disease severity and development of thrombosis in COVID-19 are mainly affected by the variation within the FVL gene. Possible FVL mutation should be investigated in COVID-19 patients and appropriate treatment should be started earlier in FVL-positive patients.
Subject(s)
COVID-19 , Thrombophilia , Thrombosis , Humans , Male , Female , Prothrombin/genetics , Risk Factors , SARS-CoV-2 , Genotype , Factor V/genetics , Thrombophilia/epidemiology , Thrombophilia/genetics , Patient Acuity , MutationABSTRACT
The development of cardiovascular disease shows increase after contracting coronavirus 2019 (COVID-19) disease and myocardial damage is observed in patients who have had the disease severely. The relationship between genetic cardiovascular risk factors with COVID-19 infection was investigated in our study. One hundred thirty-five patients, 27 of whom were COVID-19 (-) and 108 were COVID-19 (+) patients, were included in the study. Patients were divided into three groups ([COVID-19 [-], COVID-19 [+] asymptomatic, and COVID-19 [+] symptomatic + patients with pulmonary involvement]). Genetic cardiovascular risk factors were examined in blood samples taken from the patients with new generation sequencing analysis. In the clinical classification, there were no significant differences between the three groups in fibrinogen beta chain-455G>A, human platelet antigen 1 (HPA1b)/platelet receptor GPIIIa/(ITGB3) (HPA1a/b; GpIIIa; integrin beta 3 L33P), ACE I/D, AGT (M268T), AGTR1 (1166A>C), Apo E (E2/E3/E4) (rs7412, rs429358), eNOS (786T>C), eNOS (894G>T) genes (p > 0.05). However, significant differences were observed in PROCR H3 haplotype/G (endothelial protein C receptor gene [EPCR] 4600A>G [A3 haplotype]), PROCR H1 haplotype/C (EPCR 4678G>C [A1 haplotype]) genes (p < 0.05). When COVID-19 (+) and COVID-19 (-) groups were compared, it was observed that the infection was more common in people with PROCR H1 haplotype/C and PROCR H3 haplotype/G genotypes (p < 0.05). PROCR H1 and PROCR H3 haplotypes may be an important factor in contracting COVID-19 disease. In people with COVID-19 disease, revealing PROCR genetic differences and measuring sEPCR levels will be beneficial in the follow-up of the disease.