title: Increased placental antifibrinolytic potential and fibrin deposits in pregnancy-induced hypertension and preeclampsia.
abstract: Preeclampsia is characterized by maternal hypercoagulable state and intravascular coagulation, microthromboses in several organs, and impairment of uteroplacental circulation. Excessive fibrin deposition occurs in the placenta, suggesting that disorders of placental coagulation and fibrinolysis physiologic systems may have a role in hemostasis activation. Term placentas were collected from 17 hypertensive/preeclamptic women and from 17 healthy pregnant women, and processed for both histologic and hemostasis studies. Placental fibrinoid deposition was visualized by cresyl-violet staining and quantified by histomorphometric analysis. The content in hemostasis factors was measured on extracts from homogenized placentas treated by a nonionic detergent. The percentage of villi with fibrinoid deposits was higher in the diseased placentas than in controls: 13.2 +/- 11.2 versus 6.75 +/- 2.7% (p < 0.001) for the total amount of deposits; 4.8 +/- 6.7 versus 1.5 +/- 1.0% (p = 0.04) for perivillous fibrinoid deposits, which are considered as histologic markers of intraplacental fibrin. The content in type 2 plasminogen activator inhibitor (PAI-2) antigen was higher in the diseased placentas than in controls: 124 +/- 8 versus 104 +/- 6 ng/mg placental protein (p = 0.046); there was a negative correlation between PAI-2 antigen and thrombomodulin activity (r = -0.57, p = 0.02) in the diseased placentas. No significant differences were found between the two groups for placental procoagulant tissue factor and anticoagulant thrombomodulin activities, and for the content in plasminogen activators and PAI-1 antigens. Placental antifibrinolytic potential is increased in pregnancy-induced hypertension and preeclampsia. This change, and the association of the highest PAI-2 placental concentrations with the lowest concentrations of thrombomodulin, may contribute to the prethrombotic state and to the excessive placental perivillous fibrin deposition observed in these situations.
authors.affiliation: Service de Néphrologie A, Hôpital de Jour Pluridisciplinaire, Hôpital Tenon, Paris, France.
authors.forename: A
authors.initials: A
authors.lastname: Kanfer
authors.forename: J F
authors.initials: JF
authors.lastname: Bruch
authors.forename: G
authors.initials: G
authors.lastname: Nguyen
authors.forename: C J
authors.initials: CJ
authors.lastname: He
authors.forename: F
authors.initials: F
authors.lastname: Delarue
authors.forename: A
authors.initials: A
authors.lastname: Flahault
authors.forename: C
authors.initials: C
authors.lastname: Nessmann
authors.forename: S
authors.initials: S
authors.lastname: Uzan
mesh_terms: D000328:Adult; D005260:Female; D005337:Fibrin / Q000378:metabolism*; D005342:Fibrinolysis / Q000502:physiology; D006487:Hemostasis / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D010920:Placenta / Q000201:enzymology / Q000378:metabolism*; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism; D011225:Pre-Eclampsia / Q000503:physiopathology*; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000503:physiopathology*; D018180:Thrombomodulin / Q000378:metabolism
chemical_list: D017395:Plasminogen Activator Inhibitor 1; D018180:Thrombomodulin; D005337:Fibrin