Prior preterm preeclampsia and hemostatic balance in the non-pregnant state.

既往早产子痫前期和非妊娠状态下的止血平衡

阅读:4
作者:Horn Christine E, Bravo Maria Cristina, Orfeo Thomas, McLean Kelley, Bernstein Ira
OBJECTIVE: To evaluate whether a history of preterm preeclampsia (PreP) is associated with abnormal hemostatic features during the non-pregnant state, relative to people without a history of preeclampsia. STUDY DESIGN: We conducted a retrospective sub-analysis of three prospective IRB approved studies in which individuals were evaluated outside of pregnancy during the follicular phase of their menstrual cycles. We compared parameters between subjects with prior PreP (n = 21) with a combined cohort (NL, n = 74) of healthy nulliparous subjects (n = 57) and subjects with a prior normotensive pregnancy (n = 17). T-tests were employed with P < 0.05 accepted for significance. MAIN OUTCOME MEASURES: Levels of eight coagulation factors, protein C (PC), and thrombin generation (TG) were assessed in the presence or absence of thrombomodulin (TM) to evaluate the activation of the anticoagulant PC pathway. RESULTS: There were no differences in TG or factor composition between healthy nulliparous and healthy primiparous people. In contrast, the PreP cohort had increased levels of factors II, V, VII, IX, X, XI, and PC compared to the NL cohort without this history. In dynamic assays examining TG in the presence of TM, the PreP group had reduced rates (nM/min) of formation and diminished peak levels when compared to the NL group. CONCLUSIONS: Increased procoagulant factor levels are typically associated with increased TG, suggesting here that individuals with prior PreP would have a procoagulant shift in the non-pregnant state. However, the observed concurrent increase in anticoagulant PC linked with a decrease in dynamic TG suggests a possible compensatory mechanism to maintain hemostatic balance.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。