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Maternal and Fetal Outcomes in Preeclampsia: Interrelations Between Insulin Resistance, Aldosterone, Metabolic Syndrome, and Polycystic Ovary Syndrome

Cicero and colleagues have reported an interesting study on the independent determinants of maternal and fetal outcomes in a group of pregnant patients with different forms of hypertension. The diagnosis of preeclampsia (PE) and increased serum acid uric level have been found to be associated with negative maternal outcomes, while diagnosis of PE and pre-pregnancy maternal body mass index (BMI) were associated with negative fetal outcome. In both cases, the effective treatment of hypertension both during pregnancy and at delivery was a protective factor. Hypertension in pregnancy is a major risk factor for adverse outcomes both for the mother and for the fetus, and early therapeutic management is necessary not only to optimize blood pressure (BP) values but also to monitor and prevent the related complications such as metabolic syndrome, microalbuminuria, BMI, and gestational diabetes. Many studies recommend pre-pregnancy planning, therapeutic adjustments, and adequate care during and after pregnancy in women with chronic hypertension. The increase in BP in the first trimester of pregnancy, as well as the finding of an increase in BP before pregnancy, require immediate treatment and monitoring. The early management in these patients reduces the rate of complications during pregnancy and could explain the reason why only PE was found to be associated with negative outcome in the study by Cicero and colleagues. PE is the most severe form of hypertension in pregnancy, characterized by proteinuria and edema in the third trimester of pregnancy. Its pathogenesis is still debated and involves different hormonal, inflammatory, and immunologic mechanisms. PE is a characteristic complication of pregnancy, which is usually reversed after delivery and can relapse in a subsequent pregnancy. An abnormal invasion of miometrium by trophoblast is an evident alteration, but the initial cause is still unknown. The evidence of early alterations of the placental vasculature suggests that the disease has a preclinical period with few symptoms and is often not treated because BP is normal. The pathogenesis of PE is promoted by genetic and epigenetic factors and is likely related to the release into the circulation of placental factors that can activate the immune cells in an inappropriate manner. A supporting feature to this hypothesis is the development of PE in patients with hydatidiform mole in the absence of a fetus. The onset of the disease in the third trimester is sometimes dramatic and frequently associated with liver, kidney, heart, coagulation, and neurological complications, which need full treatment, careful monitoring, and often an urgent cesarean section to avoid maternal and fetal complications.