Abstract

The fetus may be exposed to increased endogenous or synthetic glucocorticoid (GS) exposure in late gestation. Approximately 7% of pregnant women in Europe and North America are treated with synthetic GSs to promote lung maturation in fetuses at risk of preterm delivery. Maternal steroid treatment before preterm delivery is one of the best documented and most cost effective life saving treatments in prenatal medicine but, in certain circumstances, the price of accelerated lung maturity may be loss of brain cells, increased neurodevelopmental disability, intra-uterine growth restriction (IUGR), and an increased risk of preterm delivery, of programming of post-natal hypertension, and of increased postnatal activity in the hypothalamo-pituitary-adrenal (HPA) axis. Placental 11β-hydroxysteroid dehydrogenase type 2 (11β- HSD2) is the key enzyme which protects the fetus from overexposure to GSs by their oxidation into inactive derivates. We review the evidence for the metabolism of GSs during pregnancy and how endogenous and synthetic GSs cause other changes in the placenta which affect fetal development.

Keywords: Antenatal exposure, glucocorticoids, 11β-hydroxysteroid dehydrogenase, metabolism, placental transport, pregnancy, fetus, synthetic glucocorticoid, steroid treatment, increased neurodevelopmental disability, intra-uterine growth restriction (IUGR), hypothalamo-pituitary-adrenal, fetal development