Objective: To evaluate whether genetic thrombophilic mutations, biochemical and biophysical indices help to predict pregnancy outcome in women with gestational hypertension.
Design and methods: A group of 59 women with gestational hypertension were prospectively tested between 24 and 26 weeks of gestation for: (i) DNA analysis to search for gene mutations of Factor V Leiden, prothrombin, methylenetetrahydrofolate reductase and plasminogen activator inhibitor type 1 (PAI-I) polymorphism; (ii) maternal serum concentrations of homocysteine and PAI-1, activated protein resistance and Factor II:C activity levels; (iii) mean uterine arterial resistance index (RI) by Doppler velocimetry; and (iv) history of hypertensive disorders in relatives (the mother and/or the father). Pregnancy outcome was evaluated, and considered 'poor' when patients developed severe pre-eclampsia, haemolysis-elevated liver enzymes-low platelets (HELLP) syndrome, fetal growth restriction (FGR), thromboembolic complications and disseminated intravascular coagulopathy (DIC).
Results: Eighteen women had a poor pregnancy outcome (11 with severe pre-eclampsia, of whom two had superimposed FGR; three with full HELLP syndrome, of whom one had DIC; four with FGR) and delivered, by emergency Caesarean section, neonates with a significantly lower mean gestational age (P < 0.0001) and birthweight (P < 0.0001). History of hypertensive disorders was significantly (P < 0.001) more common in the women group with poor (11 of 18) than normal (10 of 41) outcome. In addition, patients with a poor pregnancy outcome did not have a higher incidence of gene polymorphisms incidence, but significantly (P < 0.01) higher Factor II:C activity levels and significantly (P < 0.0001) higher mean uterine arterial RI than women with normal pregnancy outcome.
Conclusions: Only Factor II:C activity levels, uterine arterial Doppler and a history of familial hypertension are useful in predicting poor pregnancy outcome in gestational hypertension.