Oxidative Stress and Thrombophilia: Focus on Pregnancy-Related Pathophysiological Mechanisms

Thrombophilia, characterized by an increased tendency to form blood clots, presents a substantial risk during pregnancy, potentially impacting maternal and fetal outcomes. This review explores the intricate relationship between thrombophilia and oxidative stress, shedding light on their combined influence on blood clot formation. Specifically, endothelial dysfunction, driven by oxidative stress, emerges as a pivotal factor in thrombophilia, setting the stage for increased platelet activation and altered coagulation factors. Factors like Factor V Leiden mutation, Prothrombin G20210A mutation, and deficiencies in antithrombin, protein C, and protein S contribute to the pro-thrombotic state observed in thrombophilia. Furthermore, inflammation, closely intertwined with oxidative stress, exacerbates the risk of blood clot formation. Inflammatory responses lead to endothelial activation, altered endothelial function, and increased adhesion molecules expression, disrupting the delicate balance between pro- and anti-coagulant factors. Chronic inflammatory conditions, such as autoimmune disorders, potentiate a persistent state of heightened clotting risk. Additionally, impaired antioxidant defenses compound the prothrombotic state by allowing the accumulation of reactive oxygen species, thereby contributing to oxidative stress-induced endothelial dysfunction. Understanding the interplay between these factors is crucial for tailored thrombophilia management, particularly in pregnancy. Treatment strategies encompass a multifaceted approach, including anticoagulant medications, lifestyle modifications, and targeted interventions to improve endothelial health. The complex nature of thrombophilia underscores the need for a collaborative healthcare approach, involving hematologists and high-risk pregnancy specialists. Early detection, vigilant monitoring, and timely intervention are paramount in mitigating risks for both mother and baby.