Abstract
The role of plasminogen activation in the pathogenesis of preeclampsia was studied using a sensitive enzyme-linked differential immunosorbent assay to quantify α2 -plasmin inhibitor-plasmin complexes (PIP). 21 women were studied serially during pregnancy. Pregnancy was characterized by a sustained depression of PIP (P<006) lasting throughout the third trimester. No differences were found between normal pregnancies and pregnancies complicated by preeclampsia for any period of gestation. PIP levels obtained immediately prior to labor and delivery did not distinguish pregnancies complicated by preeclampsia from normal pregnancies. Regardless of the diagnosis or method of delivery, after delivery, all women had a marked rise in PIP levels within the first post-partum week (P<.001). We conclude that systemic activation of plasminogen is not central to the pathogenesis of preeclampsia and that PIP would not be useful as a predictor of impending preeclampsia. The rapid rise of PIP in the immediate post-partum period suggests that the depression of systemic plasminogen activation observed during pregnancy is affected by the feto-placental unit.