ROLE OF CYTOKINES AND THROMBOPHILIA GENES IN THE ETIOPATHOGENESIS OF ISCHEMIC STROKE AFTER COVID-19

Abstract

This article investigates the intricate interplay between cytokines and
thrombophilia genes in the etiopathogenesis of ischemic stroke following COVID19 infection. Post-COVID-19, individuals may face a pro-inflammatory state
characterized by a cytokine storm, potentially leading to endothelial dysfunction and
hypercoagulability. Concurrently, thrombophilia genes, such as Factor V Leiden and
Prothrombin G20210A mutations, can predispose individuals to thrombotic events
by disrupting the coagulation cascade. The combined effect of dysregulated
cytokines and genetic thrombophilic tendencies poses a significant risk for ischemic
stroke development post-COVID-19. Understanding the mechanisms linking
cytokine-mediated inflammation and genetic predispositions to thrombosis is crucial
for devising targeted therapeutic approaches that balance anti-inflammatory
interventions with anticoagulant strategies. This exploration into the roles of
cytokines and thrombophilia genes sheds light on the complex pathophysiology
underlying ischemic stroke occurrence in the aftermath of COVID-19, bridging the
realms of immunology, genetics, and vascular pathology