Extensive animal studies have indicated that antenatal betamethasone exposure results in
altered developmental trajectories of several fetal systems. Follow up of a randomized
controlled trial has shown that antenatal betamethasone exposure might result in insulin
resistance 30 years later. Furthermore, animal studies and randomized trials in Humans have
clearly demonstrated that betamethasone-induced growth alterations were dose-related.
In ewes, a 50% reduced dose regimen resulted in maximal improvement in preterm lamb lung
function, similar to those obtained after a full dose.
Our hypothesis is that antenatal betamethasone after a 50% dose reduction, justified by the
potential long term effects of this drug, is not inferior to a full dose to promote fetal
lung maturation in Humans.