Carmona Francisco, Lázaro Isabel, Reverter Juan C, Tàssies Dolors, Font Josep, Cervera Ricard, Balasch Juan
Institut Clínic of Gynecology, Obstetrics, and Neonatology, Barcelona, Spain.
Am J Obstet Gynecol. 2006 Feb;194(2):457-65. doi: 10.1016/j.ajog.2005.08.059.
The objective of the study was to investigate the potential role of impaired factor XII-dependent activation of fibrinolysis in treated antiphospholipid syndrome gestations developing late-pregnancy complications.
This was a prospective study in a third-level teaching hospital, including 75 patients: 25 pregnant patients having the antiphospholipid syndrome and carrying their pregnancies until 26 weeks' gestation or later (group 1); 25 pregnant patients having normal term pregnancies and delivery and no previous miscarriage (group 2); and 25 pregnant patients being diagnosed as having severe pre-eclampsia and/or intrauterine growth restriction but testing negative for antiphospholipid antibodies (group 3). Hemostatic evaluation was carried out from patients in groups 1 and 2 between 6 and 10 weeks, between 18 and 22 weeks, and between 28 and 32 weeks' gestation. Patients in group 3 were sampled between 28 and 32 weeks. An additional blood sample was obtained 4 to 6 months after delivery (baseline). The Mann-Whitney U test, the Friedman test, and the chi2 test were used.
Patients in group 1 were characterized by increased factor VIIa levels, increased prothrombin fragment 1+2 levels, reduced factor XIIa levels, diminished functional urokinase-type plasminogen activator levels, and decreased levels of plasmin/alpha-2-plasmin inhibitor complexes. These abnormalities were more evident in patients in group 1 developing pre-eclampsia and/or intrauterine growth restriction.
Impaired factor XIIa-dependent activation of fibrinolysis seems to be a key mechanism related to late-pregnancy complications in patients with the antiphospholipid syndrome.
本研究的目的是探讨凝血因子XII依赖性纤维蛋白溶解激活受损在患有抗磷脂综合征的妊娠中发生晚期妊娠并发症的潜在作用。
这是一项在三级教学医院进行的前瞻性研究，包括75名患者：25名患有抗磷脂综合征且妊娠持续至妊娠26周或更晚的孕妇（第1组）；25名足月妊娠并分娩且既往无流产史的孕妇（第2组）；以及25名被诊断为重度子痫前期和/或胎儿生长受限但抗磷脂抗体检测阴性的孕妇（第3组）。对第1组和第2组的患者在妊娠6至10周、18至22周以及28至32周进行止血评估。第3组的患者在28至32周进行采样。在分娩后4至6个月获取额外的血样（基线）。使用曼-惠特尼U检验、弗里德曼检验和卡方检验。
第1组患者的特征为凝血因子VIIa水平升高、凝血酶原片段1+2水平升高、凝血因子XIIa水平降低、功能性尿激酶型纤溶酶原激活剂水平降低以及纤溶酶/α-2-纤溶酶抑制剂复合物水平降低。这些异常在发生子痫前期和/或胎儿生长受限的第1组患者中更为明显。
凝血因子XIIa依赖性纤维蛋白溶解激活受损似乎是抗磷脂综合征患者晚期妊娠并发症的关键机制。
