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Low catechol-O-methyltransferase and 2-methoxyestradiol in preeclampsia: more than a unifying hypothesis.

Preeclampsia is a systemic disorder of pregnancy characterized by widespread maternal endothelial dysfunction. Clinical manifestations of preeclampsia include placental hypoxia, hypertension, proteinuria and fluid retention. The condition is common and affects over 5% of all pregnancies, thus remaining a leading cause of maternal and fetal morbidity and mortality worldwide [1]. Pregnancies complicated by preeclampsia are associated with greater risk and earlier onset of cardiovascular disease in both mother and infant [2,3]. Preeclampsia originates in the placenta, as it may occur only in the presence of placenta or a hydatiform mole and resolves dramatically postpartum after the delivery of the placenta. Generalized endothelial dysfunction resulting in vasoconstriction and end-organ ischaemia is attributed in all of the clinical aspects of the maternal syndrome in preeclampsia. Search for a unique circulating factor [4] resulted in an identification of multiple factors of endothelial dysfunction, activation and oxidative stress. A major breakthrough was achieved during the past five years by a series of experimental and clinical studies from Karumanchi and associates implicating that changes in circulating angiogenic factors play a decisive role in the pathogenesis of preeclampsia (reviewed in [5]). Increased expression of soluble fms-like tyrosine kinase 1 (sFlt1), a variantofthemembrane-boundvascularendothelialgrowth factor (VEGF)-receptor 1 that consists of the extracellular ligand-binding domain, was associated with decreased placental growth factor (PIGF) and VEGF signalling and consecutive defective angiogenesis [6]. Soluble Flt1 acts as a natural antagonist of the circulating VEGF and increases from mid-gestation onwards, to reach the peak 5–8 weeks before the onset of the maternal syndrome [7]. Soluble