Objective: To evaluate the behavior of activators and inhibitors of the hemostatic system in hypertensive pregnant women compared with normal pregnant women. Methods: Three groups of patients were enrolled: 54 normal pregnant women followed longitudinally from the first to the third trimester, 21 hypertensive third trimester pregnant women (14 with the diagnosis of gestational hypertension and 7 with the diagnosis of preeclampsia), and 45 healthy non-pregnant women. Peripheral venous blood samples were assayed for total alkaline phosphatase, placental alkaline phosphatase (FLAP), uric acid (UA), prothrombin time, partial thromboplastin time, fibrinogen, antithrombin III (AT III), protein C, protein S, tissue plasminogen activator, plasminogen activator inhibitor type 1 (PAI), and prothrombin activation fragment F1 + 2 (F1 + 2). Results: Only FLAP and t-PA levels were significantly higher in the hypertensive women group compared with the normal pregnant women group. AT III activity was significantly reduced in hypertensive pregnancies compared with normal non-pregnant women. In the hypertensive group there was a significant correlation between UA and F1 + 2 levels (r = 0.4881, P < 0.05). Similar results were obtained when F1 + 2 values were correlated with PAI-1 values (r = 0.3146, P < 0.05). A positive correlation existed between PAI-1 and FLAP activity. There was a negative correlation between AT III and UA (r = 0.565, P = 0.0028). Uric acid levels, FLAP, PAI-1, and F1 + 2 concentrations were significantly higher in the preeclamptic subgroup than in the women with a diagnosis of gestational hypertension. Conclusions: These data suggest that F1 + 2 may be a sensitive marker of a complicated pregnancy-induced hypertensive state. However, only when the increase of F1 + 2 is associated with pathological FLAP and PAI-1 levels, should it be considered consistent with severe worsening of disease because activation of coagulation is no longer compensated.

Coagulation and fibrinolytic parameters in normal and hypertensive pregnancies

RICCI, GIUSEPPE;GUASCHINO, SECONDO
1997-01-01

Abstract

Objective: To evaluate the behavior of activators and inhibitors of the hemostatic system in hypertensive pregnant women compared with normal pregnant women. Methods: Three groups of patients were enrolled: 54 normal pregnant women followed longitudinally from the first to the third trimester, 21 hypertensive third trimester pregnant women (14 with the diagnosis of gestational hypertension and 7 with the diagnosis of preeclampsia), and 45 healthy non-pregnant women. Peripheral venous blood samples were assayed for total alkaline phosphatase, placental alkaline phosphatase (FLAP), uric acid (UA), prothrombin time, partial thromboplastin time, fibrinogen, antithrombin III (AT III), protein C, protein S, tissue plasminogen activator, plasminogen activator inhibitor type 1 (PAI), and prothrombin activation fragment F1 + 2 (F1 + 2). Results: Only FLAP and t-PA levels were significantly higher in the hypertensive women group compared with the normal pregnant women group. AT III activity was significantly reduced in hypertensive pregnancies compared with normal non-pregnant women. In the hypertensive group there was a significant correlation between UA and F1 + 2 levels (r = 0.4881, P < 0.05). Similar results were obtained when F1 + 2 values were correlated with PAI-1 values (r = 0.3146, P < 0.05). A positive correlation existed between PAI-1 and FLAP activity. There was a negative correlation between AT III and UA (r = 0.565, P = 0.0028). Uric acid levels, FLAP, PAI-1, and F1 + 2 concentrations were significantly higher in the preeclamptic subgroup than in the women with a diagnosis of gestational hypertension. Conclusions: These data suggest that F1 + 2 may be a sensitive marker of a complicated pregnancy-induced hypertensive state. However, only when the increase of F1 + 2 is associated with pathological FLAP and PAI-1 levels, should it be considered consistent with severe worsening of disease because activation of coagulation is no longer compensated.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11368/2757955
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