Preeclampsia – More than a pregnancy complication

Abstract

Preeclampsia and intrauterine growth restriction (IUGR) account for a major part of perinatal and maternal morbidity worldwide and are associated with increased later cardiovascular risk. Both diseases are characterized by a shallow endovascular trophoblast invasion causing a disturbed placental development and are considered as syndromes with numerous vascular, metabolic, immunological and clinical alterations. Their etiology and pathophysiological consequences remain mostly unresolved. Beside others one hypothesis favors oxidative stress as a relevant pathophysiological factor. Oxidative stress as an imbalance between free radicals and the capacity of protective antioxidant systems is thought to be a potent promoter of maternal vascular dysfunction and endothelial damage. As both pregnancy complications furthermore are associated with an increased later cardiovascular risk for mother and child, the pathobiology mediated by oxidative stress may have general and long-term devastating influence on vascular function.

Disturbed trophoblast invasion and placental development cause an abnormal uterine perfusion in mid-pregnancy, which is easily detectable by abdominal ultrasound and identifies women at risk for the mentioned pregnancy complications antedating their clinical manifestation. We showed that an abnormal uterine perfusion in pregnancy is characterized by a decreased maternal plasma antioxidant capacity. Even though this reduction is not related to the clinical outcome of these high-risk pregnancies, oxidative stress and uterine perfusion are clearly pathophysiologically connected.

In this article, we focus on links between oxidative stress and uterine perfusion and possible implications for the early detection of patients at risk for preeclampsia and IUGR. This might improve our understanding of these relationships, and may become of beneficial impact for the short- and long-term outcome in affected mothers and their children.