VanWijk Marja J, Boer Kees, Berckmans René J, Meijers Joost C M, van der Post Joris A M, Sturk Augueste, VanBavel Ed, Nieuwland Rienk
Department of Obstetrics, Academic Medical Center, Amsterdam, The Netherlands.
Thromb Haemost. 2002 Sep;88(3):415-20.
Coagulation activation in pregnancy is further enhanced in preeclampsia. We investigated whether this results from increased thrombin generation by the plasma itself or its cell-derived microparticles. Plasma samples were obtained from preeclamptic, normal pregnant and nonpregnant women (each n = 10). Prothrombin fragment 1+2 (F1+2) and thrombin-antithrombin complex (TAT) concentrations were increased in pregnancy and further increased in preeclampsia. In pregnancy and preeclampsia, increased activated protein C resistance occuffed (APC sensitivity ratio: 3.3 +/- 0.8 and 2.5 +/- 0.8, both P <0.001 vs. nonpregnant). In normal pregnant microparticle-free plasma the thrombin generation correlated with TAT (r = 0.84, P = 0.005) and APC resistance correlated with F1+2 (r = 0.68, P = 0.04). In preeclampsia thrombin generation by plasma was increased (P = 0.005), independent of APC resistance. Thrombin generation by microparticles was similar in all groups, although different coagulation activation pathways were utilized, indicating that circulating microparticles are not directly involved in coagulation activation in pregnancy and preeclampsia. In contrast, APC resistance can explain coagulation activation in pregnancy, while enhanced coagulation activation in preeclampsia results, in part, from an increased thrombin generating capacity of plasma independent of APC resistance.
子痫前期患者孕期的凝血激活进一步增强。我们研究了这是否源于血浆本身或其细胞衍生的微粒产生的凝血酶增加。从子痫前期、正常妊娠和非妊娠女性中获取血浆样本（每组n = 10）。妊娠时凝血酶原片段1 + 2（F1 + 2）和凝血酶 - 抗凝血酶复合物（TAT）浓度升高，子痫前期时进一步升高。在妊娠和子痫前期，活化蛋白C抵抗增加（APC敏感性比值：分别为3.3±0.8和2.5±0.8，与非妊娠组相比，P均<0.001）。在正常妊娠的无微粒血浆中，凝血酶生成与TAT相关（r = 0.84，P = 0.005），APC抵抗与F1 + 2相关（r = 0.68，P = 0.04）。子痫前期时，血浆凝血酶生成增加（P = 0.005），与APC抵抗无关。微粒产生的凝血酶在所有组中相似，尽管使用了不同的凝血激活途径，这表明循环微粒不直接参与妊娠和子痫前期的凝血激活。相比之下，APC抵抗可解释妊娠时的凝血激活，而子痫前期增强的凝血激活部分源于血浆凝血酶生成能力增加，与APC抵抗无关。
