THROMBOEMBOLIC COMPLICATIONS IN COVID-19: THE ROLE OF GENETIC MUTATIONS IN THE HYPERCOAGULABLE STATE
DOI:
https://doi.org/10.56238/levv16n55-151Keywords:
COVID-19, Complications, Hypercoagulability, Mutations, ThromboembolismAbstract
Introduction: COVID-19, the disease caused by the SARS-CoV-2 virus, has been associated with several systemic complications, among which thromboembolic complications stand out, such as pulmonary thromboembolism, identified among patients admitted to intensive care units (ICUs), presenting a high mortality rate. Upon infecting the individual, the virus generates a state of hypercoagulability, which, in the presence of risk factors such as the MTHFR gene mutation, as well as Factor V Leiden, predisposes to vascular alterations with consequent development of thromboembolic events. Therefore, it becomes relevant to seek the relationship between the vascular complications of COVID-19 and genetic factors that may predispose to these conditions. General objective: In this sense, the objective of this study was to contextualize thromboembolic complications during infection by the SARS-CoV-2 virus. Methodology: A literature review was conducted using a manual search of scientific articles published between 2019 and 2024 on the Scielo and PubMed platforms, using the association between SARS-CoV-2 infection and thromboembolic events as an inclusion criterion. Results: The results demonstrated a strong association between endotheliitis caused by the infection and genetic factors that lead to hypercoagulability, resulting in vascular complications and thromboembolic events. SARS-CoV-2 infects host cells through its binding to angiotensin-converting enzyme 2 (ACE2) in pneumocytes and endothelial cells, leading to downregulation of the enzyme and elevating serum angiotensin II levels. Infection with the virus activates innate immunity, with the production of interferons, which attract macrophages secreting pro-inflammatory cytokines such as IL-1, IL-6, and TNF-α. Among the most cited mutations, the C677T polymorphism of the methylenetetrahydrofolate reductase (MTHFR) gene stands out, leading to hyperhomocysteinemia, as well as the G1691A mutation of the factor V gene, one of the main causes of resistance to activated protein C (APC). Both compromise the coagulation cascade, leading to thrombophilia. To demonstrate the hypercoagulable state, D-dimer, a fibrin degradation product, has been widely cited in studies as a prognostic marker and has been shown to be especially elevated in patients already in more critical states within ICUs. Conclusion: Thus, it is possible to establish the relationship between infection with the SARS-CoV-2 virus and thromboembolic events causing multiple complications. The mechanisms and mutations are still being investigated and detailed to identify earlier and more effective biomarkers of the prothrombotic state in infected patients.
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