Abstract
Aim: This study aimed to investigate the relationship between severe novel coronavirus pneumonia (NCP) and hypercoagulable conditions that predispose patients to thrombosis such as the prothrombin gene (F2) rs1799963 (G20210A), factor V Leiden (F5) rs6025 (G1691A) and PAI-1 (rs1799768). Patients: NCP-diagnosed 62 previously healthy patients were enrolled for the investigation of the thrombophilia-related polymorphisms. Materials & methods: The frequency of genotypes were compared with healthy control group frequencies from other studies. Results: There were no statistically significant differences between the severe patient group and the healthy population regarding the investigated single nucleotide polymorphisms (SNPs). Conclusion: This study is the first to rule out the relationship of rs1799963, rs6025 and rs1799768 with severe NCP.
Highlights
Result62 patients who met the criteria during the study were included in the study. The mean (± standard deviation) of age was 38.83 ± 11.04 (minimum 18, maximum 60) years
It is known that there is a relationship between severe novel coronavirus pneumonia (NCP) and hypercoagulable conditions that predispose patients to thrombosis
The prothrombin gene (F2 rs1799963/G20210A), factor V Leiden (F5 rs6025/G1691A) and PAI-1 are important polymorphic biomarkers of thrombophilia that are investigated in severe NCP patients within this study
Summary
62 patients who met the criteria during the study were included in the study. The mean (± standard deviation) of age was 38.83 ± 11.04 (minimum 18, maximum 60) years. There was no significant difference between groups regarding the prevalence of rs1799963 (F2) and rs6025 (F5 Leiden) (Table 1). While there was a statistically significant difference between groups in the prevalence of rs1799768 (PAI-1 it was considered a coincidence and nonimportant finding because of the small sample size; upon further review, it was observed that the main cause of the difference between groups was the low prevalence of 5G/5G (12.6%) in one of the control groups [7], which did not support our hypothesis (Figure 1). There was no significant difference between groups in the prevalence of the 4G/4G genotype. No significant difference between groups in the prevalence of 4G/4G genotype which is correlated with increased thrombosis risk was observed
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