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近年研究,许多不良妊娠的患者具有血栓形成倾向,这种因遗传性或基因突变所致的持续高凝状态而引起血栓形成风险增加称为遗传性易栓症(thrombophilia)。不良妊娠包括妊娠期高血压综合征(如先兆子痫)、胎盘早剥、胎儿生长受限、死胎及不明原因的习惯性流产等。易栓症不一定在临床上表现为显性血栓性疾病,但可能会因凝血-抗凝机制或纤溶活性失衡,子宫螺旋动脉或绒毛血管微血栓形成,导致胎盘灌注不良甚至梗塞,从而发生不良妊娠。与不良妊娠相关的遗传性易栓症包括蛋白S(PS)及蛋白C(PC)和抗凝血酶缺乏,促凝因子的异常如FV Leidn和凝血酶原基因G202010A突变,亚甲基四氢叶酸还原酶(MTHFR)基因C677T突变和纤溶酶原激活物抑制物-1(PAI-1)基因多态性等。本文旨在阐述伴有遗传性易栓症背景下不良妊娠发生的机制,两者之间的相关性,以及如何预防和治疗妊娠相关的血栓事件。
In recent years, many patients with adverse pregnancy have thrombophilia. The increased risk of thrombosis caused by the persistent hypercoagulable state caused by genetic or genetic mutation is called thrombophilia. Unfavorable pregnancies include gestational hypertension (such as preeclampsia), placental abruption, fetal growth restriction, stillbirth and unexplained habitual abortion. Thrombophilia does not necessarily appear clinically manifest as a thrombotic disease, but may occur due to an imbalance in the coagulation-anticoagulation mechanism or fibrinolytic activity, uterine spiral artery or villus microvascular thrombosis, leading to poor or even obstructed placental perfusion. Bad pregnancy. Hereditary thromboses associated with adverse pregnancy include protein S (PS) and protein C (PC) and antithrombin deficiency, abnormalities of procoagulant factors such as FV Leidn and the prothrombin gene G202010A mutation, methylenetetrahydrogen C677T mutation in folic acid reductase (MTHFR) gene and plasminogen activator inhibitor-1 (PAI-1) gene polymorphism. This article aims to elucidate the mechanisms underlying adverse pregnancy in the context of hereditary thrombophilia, the correlation between the two, and how to prevent and treat pregnancy-related thrombotic events.