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

Year 2024, Volume: 7 Issue: 6, 649 - 653, 27.10.2024

Esma Sevil Akkurt , Sertan Bulut , Tuğçe Şahin Özdemirel , Nihal Mutlu , Kerem Ensarioğlu , Berna Akıncı Özyürek

https://doi.org/10.32322/jhsm.1546963

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

References

• World Health Organization. Coronavirus disease 2019 (COVID-19): Situation Report, 51. 2020. Available at: https://apps.who.- int/iris/handle/10665/331475. Accessed July 15, 2020.
• Giordano NJ, Jansson PS, Young MN, Hagan KA, Kabrhel C. Epidemiology, pathophysiology, stratification, and natural history of pulmonary embolism. Tech Vasc Interv Radiol. 2017; 20(3):135-140.
• Katneni UK, Alexaki A, Hunt RC, et al. Coagulopathy and thrombosis as a result of severe COVID-19 infection: a microvascular focus. Thromb Haemost. 2020;120(12):1668-1679.
• Niculae CM, Hristea A, Moroti R. Mechanisms of COVID-19 associated pulmonary thrombosis: a narrative review. Biomedicines. 2023;11(3):929.
• Nakashima MO, Rogers HJ. Hypercoagulable states: an algorithmic approach to laboratory testing and update on monitoring of direct oral anticoagulants. Blood Res. 2014;49(2): 85-94.
• Chung I, Lip GY. Virchow’s triad revisited: blood constituents. Pathophysiol Haemost Thromb. 2003;33(5-6):449-454.
• Sayinalp N, Haznedaroğlu IC, Aksu S, et al. The predictability of factor V Leiden [FV:Q(506)] gene mutation via clotting-based diagnosis of activated protein C resistance. Clin Appl Thromb Hemost. 2004;10(3):265-270.
• Jadaon MM. Epidemiology of prothrombin G20210A mutation in the mediterranean region. Mediterr J Hematol Infect Dis. 2011; 3(1):e2011054.
• Katsoularis I, Fonseca-Rodríguez O, Farrington P, et al. Risks of deep vein thrombosis, pulmonary embolism, and bleeding after covid-19: nationwide self-controlled cases series and matched cohort study. BMJ. 2022;377:e069590.
• Di Minno A, Ambrosino P, Calcaterra I, Di Minno MND. COVID-19 and venous thromboembolism: a meta-analysis of literature studies. Semin Thromb Hemost. 2020;46(7):763-771.
• Mo P, Xing Y, Xiao Y, et al. Clinical characteristics of refractory Coronavirus disease 2019 in Wuhan, China. Clin Infect Dis. 2021;73(11):e4208-e4213.
• Wu C, Chen X, Cai Y, et al. Risk factors associated with acute respiratory distress syndrome and death in patients with Coronavirus disease 2019 pneumonia in Wuhan, China. JAMA Intern Med. 2020;180(7):1031.
• Chen G, Wu D, Guo W, et al. Clinical and immunological features of severe and moderate coronavirus disease 2019. J Clin Invest. 2020;130(05):2620-2629.
• Huang C, Wang Y, Li X, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet. 2020;395(10223):497-506.
• Levi M, Thachil J, Iba T, Levy JH. Coagulation abnormalities and thrombosis in patients with COVID-19. Lancet Haematol. 2020;7(06):e438-e440.
• Loo J, Spittle DA, Newnham M. COVID-19, immunothrombosis and venous thromboembolism: biological mechanisms. Thorax. 2021;76:412-420.
• Han H, Yang L, Liu R, et al. Prominent changes in blood coagulation of patients with SARS-CoV-2 infection. Clin Chem Lab Med. 2020;58:1116-1120.
• Aydin S, Ugur K, Yalcin H, et al. Overview of COVID-19’s relationship with thrombophilia proteins. Turk J Biochemist. 2021;46(6):609-622. doi:10.1515/tjb-2021-0183
• Frydman GH, Boyer EW, Nazarian RM, Van Cott EM, Piazza G. Coagulation status and venous thromboembolism risk in African Americans: a potential risk factor in COVID-19. Clin Appl Thromb Hemost. 2020;26:1076029620943671. doi:10.1177/ 1076029620943671
• Stefely, JA, Christensen, BB, Gogakos, T, et al. Marked factor V activity elevation in severe COVID-19 is associated with venous thromboembolism. Am J Hematol. 2020;95:1522-1530. doi:10. 1002/ajh.25979
• Xie J, Prats-Uribe A, Feng Q, et al. Clinical and genetic risk factors for acute incident venous thromboembolism in ambulatory patients with COVID-19. JAMA Intern Med. 2022;182(10):1063-1070. doi:10.1001/jamainternmed.2022.3858
• Tse J, Gongolli J, Prahlow JA. Hereditary thrombophilia as a possible risk factor for severe disease in COVID-19: a case series. Forensic Sci Med Pathol. 2024. doi:10.1007/s12024-024-00879-4