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To evaluate whether genetic thrombophilic mutations, biochemical and biophysical indices help to predict pregnancy outcome in women with gestational hypertension.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).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.Only Factor II:C activity levels, uterine arterial Doppler and a hystory of familial hypertension are useful in predicting poor pregnancy outcome in gestational hypertension.