Physiopathology of pre-eclampsia

Pre-eclampsia is a pregnancy-specific disorder that presents major health problems for both mothers and babies. It is a major cause of maternal mortality, especially in developing countries, where it may account for 80% of maternal deaths. In this review we have discussed the putative pathogenetic mechanisms of this severe illness. Review of the international literature on pre-eclampsia. Pre-eclampsia occurs predominantly in primigravidas and is associated with increased foetal and maternal risk. Generally speaking, one could hypothesise that during pre-eclampsia the oxidative, coagulative and vasomotor balance is altered by increased sensitivity to angiotensin II associated with reduced synthesis of vasodilator prostaglandins, sympathetic nervous system hyperactivity, hyperlipidaemia associated with raised lipoperoxide synthesis and incomplete implant of cytotrophoblast in maternal spiral arteries. General vasoconstriction could then be a consequence with related utero-placental ischaemia and endothelial damage. These features are clinically characterised by arterial hypertension, proteinuria and sodium retention. The predisposition to develop pre-eclampsia seems to be at least partially hereditary and the risk seems to be transmissible through male sons. To explain the susceptibility of some women to develop pre-eclampsia, specific genetic polymorphisms have been associated to increased risk. Many factors are involved in the pathogenesis of pre-eclampsia. Occasionally these factors seem to act together, sometimes they do not and, consequently, it might be difficult to postulate a common pathogenesis for the disorder. Good obstetrical practice will identify known risk factors but will not enable physicians to determine the risk value for a particular pregnancy. Moreover, we are far from understanding the exact mechanisms involved, let alone acting upon them. The achievement of these objectives constitute a remarkable challenge for research.