Predictive Values of Coagulation/Fibrinolysis Parameters for the Termination of Pregnancy Complicated by Severe Preeclampsia

ABSTRACT

We investigated coagulation/fibrinolysis parameters for significant differences between patients with early-onset severe preeclampsia (< 32 weeks gestation, wG) and those with late-onset severe preeclampsia (≥ 32 wG). A decrease in antithrombin (AT), protein C (PC), and free protein S (PS) activities and an increase in plasmin-α2-plasmin inhibitor complex (PIC), thrombin-antithrombin complex (TAT), and FDP D-dimer (D-dimer) were observed. However, there were no statistical differences between the two groups. Once preeclampsia occurred and it developed severe, the changes in coagulation/fibrinolysis parameters became more severe in spite of early-onset preeclampsia or late-onset preeclampsia. We also investigated coagulation/fibrinolysis abnormalities in 101 patients with severe preeclampsia. A significant increase in WBC, RBC, Hb, Ht, TAT, PIC, and D-dimer and a significant decrease in platelet (Plt) counts and AT activity were observed. ΔPlt (the difference between platelet counts in early gestation and before delivery) was -5.0 × 10

@affil4:⁴ /μL in cases with severe preeclampsia. Among patients with severe preeclampsia, coagulation/fibrinolysis changes before delivery were typical for patients with cesarean section compared with those with successful vaginal delivery. These facts suggest that an excessive hypercoagulable state is associated with the termination of pregnancy resulting from the aggravation of preeclampsia. From the viewpoint of coagulation/fibrinolysis changes, the termination of pregnancy could be recommended when the levels of parameters exceed the following values; ΔPlt >| -6.0 | × 10

@affil4:⁴ /μL, D-dimer > 4 μg/mL, AT activity < 79%, TAT > 26 ng/mL, and PIC > 1.2 μg/mL. Particularly, ΔPlt and D-dimer are useful bedside predictive markers in order to decide the optimal time for the termination of pregnancy in patients with severe preeclampsia.

KEYWORD

Preeclampsia - platelet counts - FDP D-dimer - antithrombin - thrombin-antithrombin complex

REFERENCES

• 1 Matsuda Y, Tomosugi T, Maeda Y. Cerebral magnetic resonance angiographic findings in severe preeclampsia.  Gynecol Obstet Invest . 1995;  40 249-252
• 2 Kobayashi T, Terao T. Preeclampsia as chronic disseminated intravascular coagulation.  Gynecol Obstet Invest . 1987;  24 170-178
• 3 Kelton J G, Hunter D JS, Neame P B. A platelet function defect in pre-eclampsia.  Obstet Gynecol . 1985;  65 107-109
• 4 Kobayashi T, Tokunaga N, Sugimura M. Coagulation/fibrinolysis disorder in patients with severe preeclampsia.  Semin Thromb Hemost . 1999;  25 451-454
• 5 Chen J, Ishii M, Wang L, Ishii K, Coughlin S R. Thrombin receptor activation.  J Biol Chem . 1994;  269 16041-16045
• 6 Rbiet M J, Plantier J L, Dejana E. Thrombin-induced endothelial cell dysfunction.  Br Med Bull . 1994;  50 936-945
• 7 Khatun S, Kanayama N, Belayet H. The impact of vasoactive peptides on nitric oxide production in cultured sympathetic neurons.  Neuroscience . 1999;  93 605-609
• 8 Khatun S, Kanayama N, Belayet H. Increased concentrations of plasma neuropeptide-Y in patients with eclampsia and preeclampsia.  Am J Obstet Gynecol . 2000;  182 896-900
• 9 Page N M, Woods R J, Gardiner S M. Excessive placental secretion of neurokinin B during the third trimester causes pre-eclampsia.  Nature . 2000;  405 797-800
• 10 Terao T, Kobayashi T, Imai N, Oda H, Karasawa T. Pathological state of the coagulatory and fibrinolytic system in preeclampsia and the possibility of its treatment with AT-III concentrate.  Asia Oceania J Obstet Gynecol . 1989;  15 25-32
• 11 Maki M, Kobayashi T, Terao T. Antithrombin therapy for severe preeclampsia: Results of a double blind, randomized, placebo-controlled trial.  Thromb Haemost . 2000;  84 583-590
• 12 Dekker G A, de Vries I P J, Doelitzsch P M. Underlying disorders associated with severe early-onset preeclampsia.  Am J Obstet Gynecol . 1995;  173 1042-1048