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Hemostatic variables as independent predictors for fetal growth retardation in preeclampsia
R Schjetlein1, M Abdelnoor, G Haugen
1Hematological Research Laboratory, Ullevål University Hospital, Oslo, Norway.
Insights
Preeclampsia and fetal growth retardation (FGR) are linked to placental issues. Low levels of plasminogen activator inhibitor type-2 (PAI-2) antigen in plasma are a consistent risk factor for both conditions.
Area of Science:
- Obstetrics and Gynecology
- Hematology
- Perinatal Medicine
Background:
- Preeclampsia and fetal growth retardation (FGR) are significant contributors to perinatal morbidity.
- Intravascular coagulation, placental fibrin deposition, and hypoperfusion are implicated in these pregnancy complications.
Purpose of the Study:
- To investigate the association between hemostatic and lipid metabolism variables and preeclampsia and FGR.
- To identify key predictors for preeclampsia, FGR, and low birth weight.
Main Methods:
- Examined hemostatic and lipid metabolism variables in 200 women with preeclampsia and 97 normotensive controls.
- Utilized univariate and multivariate regression models to analyze associations with preeclampsia and FGR.
Main Results:
- Elevated plasma levels of thrombin-antithrombin complex (TAT) and tissue factor pathway inhibitor free antigen (TFPI-Fag) were observed in preeclampsia.
- Decreased plasma levels of antithrombin (AT) and PAI-2 antigen were associated with preeclampsia and FGR.
- Low PAI-2 antigen levels, placental infarction, and low maternal weight predicted low birth weight.
Conclusions:
- Findings support the hypothesis of activated coagulation in placental vessels in preeclampsia.
- Low plasma PAI-2 antigen concentration is identified as a consistent risk factor for preeclampsia and FGR.
Background:
Preeclampsia is a major contributor to perinatal disease and fetal growth retardation (FGR). It has been suggested that increased intravascular coagulation, fibrin deposition in spiral arteries and hypoperfusion of the placenta are involved in these pregnancy complications.
Methods:
Multiple variables of the hemostatic system and lipid metabolism, as well as clinical features, were entered into univariate and multivariate models in order to examine the association with preeclampsia and FGR.
Results:
Two hundred women with preeclampsia and 97 normotensive pregnant women were examined. Plasma levels of the thrombin-antithrombin complex (TAT), tissue factor pathway inhibitor free antigen (TFPI-Fag), protein S free antigen, plasminogen activator inhibitor type-1 (PAI-1) activity and serum levels of triglycerides were significantly increased, whereas plasma levels of antithrombin (AT), fibrinogen, C4b-binding protein (C4b-BP), PAI-2 antigen and serum HDL-cholesterol levels were decreased in the presence of preeclampsia. In the multivariate regression analysis, high TFPI-Fag plasma levels were associated with the presence of preeclampsia. The presence of FGR was in the univariate analysis associated with decreased PAI-1 activity and lower concentrations of fibrin, fibrinogen, factor VII antigen and PAI-2 antigen, as well as with evidence of macroscopic placental infarction. In a multivariate regression model, low maternal weight, placental infarction and low PAI-2 levels were predictors for low birth weight. In a logistic regression model, with the presence or absence of FGR as the dependent variable, male sex of the infant, placental infarction, low PAI-1 activity and factor VII antigen or PAI-2 antigen levels were independent predictors.
Conclusions:
Our results are consistent with activated coagulation in the placental vessels in preeclampsia. A low concentration of PAI-2 antigen in plasma emerged as the most consistent risk factor for preeclampsia and FGR.