A. Dimitrijevic, V. Jakovljevic, N. Jovic, J. Djuric, K. Andric, J. J. Jovic
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引用次数: 0
Abstract
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.
血栓性疾病(Thrombophilia)的特点是容易形成血凝块,在妊娠期间具有很大的风险,可能会影响母体和胎儿的预后。本综述探讨了血栓性疾病与氧化应激之间错综复杂的关系,揭示了它们对血凝块形成的共同影响。具体来说,氧化应激导致的内皮功能障碍是血栓性疾病的一个关键因素,为血小板活化增加和凝血因子改变创造了条件。因子 V Leiden 突变、凝血酶原 G20210A 突变以及抗凝血酶、蛋白 C 和蛋白 S 缺乏等因素,都会导致血栓性疾病中的血栓形成。此外,炎症与氧化应激密切相关,会加剧血栓形成的风险。炎症反应会导致内皮活化、内皮功能改变和粘附分子表达增加,从而破坏促凝因子和抗凝因子之间的微妙平衡。慢性炎症(如自身免疫性疾病)会加剧凝血风险的持续状态。此外,抗氧化防御功能受损也会导致活性氧的积累,从而加剧氧化应激引起的内皮功能障碍,从而加重促血栓形成状态。了解这些因素之间的相互作用对于有针对性地治疗血栓性疾病,尤其是妊娠期血栓性疾病至关重要。治疗策略包括多方面的方法,包括抗凝药物、生活方式调整以及改善内皮健康的针对性干预措施。血栓性疾病的复杂性突出表明,需要血液科医生和高危妊娠专科医生共同协作的医疗保健方法。早期发现、警惕监测和及时干预对于降低母婴风险至关重要。