Is there a role of genetic tendency in post-COVID pulmonary thromboembolism?

Abstract

Aims: COVID-19 is a multisystemic disease characterized by endothelial dysfunction. The improper activation of the coagulation cascade may lead to thromboembolic events, which are presumed to contribute to the disease’s overall high morbidity and mortality. This research examines the role of thrombophilia mutations in patients diagnosed with post-COVID pulmonary thromboembolism. Methods: Between May 2020 and December 2020, 61 patients were diagnosed with pulmonary thromboembolism (PTE). Thirty-two patients were positive in COVID-19 -RT-PCR testing, and 29 patients were identified with non-COVID PTE. All PTE diagnoses were made by thorax computed tomographic angiography. Demographic characteristics, genetic mutation results, and laboratory values of the patients were retrospectively evaluated. Results: The median age of patients was 56 years (25-81), and most patients (n=43,70.5%) were male. There was no difference between factor 5 Leiden mutation, while prothrombin 20210A mutation was more commonly observed in post-COVID patients (p<0.05). Between the two groups, no difference was observed regarding MTHFR gene mutation, anticardiolipin and antiphospholipid antibodies, protein S, and protein C values. D-dimer values were statistically higher in the post-COVID PTE group (p<0.05). As seen in the study, we may state that patients with post-COVID PTE had a higher diagnosed prothrombin 20210A and more elevated D-dimer values compared to non-COVID-related PTE patients. Conclusion: In our study, we found that D-dimer values ​​were higher in patients with post-COVID PTE than in patients with non-COVID PTE, and prothrombin 20210A mutation was more common in the post-COVID PTE patient group. We believe that further studies with a larger study group are needed to elucidate this issue.

Keywords

• COVID-19
• D-dimer
• factor 5 Leiden mutation
• post-COVID pulmonary thromboembolism
• thrombophilia mutations

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