UC Irvine

Objective: We examined the hypothesis that a single course of antenatal betamethasone influences the maternal-fetal insulin-IGF-GH axis. Design: A prospective, observational, pilot study consisting of four groups of pregnant women: (1) received betamethasone and delivered 2 weeks post treatment; (III) untreated women who delivered 37 weeks (term controls). Maternal and mixed umbilical cord blood was collected at delivery and analyzed for insulin, glucose, IGF-I IGF-II, IGFBP-1, IGFBP-3, GH and GHBP. Results: Betamethasone increased maternal insulin, glucose and IGF-I levels without affecting IGFBPs. In the fetal compartment, betamethasone treatment was associated with a delayed suppressive effect on GH and a sustained suppressive effect on IGF-II levels. There were no differences in infant size or neonatal morbidities between patients who delivered 2 weeks post betamethasone treatment. In Group IV, birth weight correlated positively with cord IGF-I levels (r(2) = 0.41, p = 0.0098) and negatively with cord IGFBP-1 levels (r(2) = 0.51, p = 0.0039), and ponderal index correlated negatively with cord IGFBP-1 levels (r(2) = 0.27, p < 0.05). Conclusions: A single course of antenatal betamethasone influences the maternal-fetal insulin-IGF-GH axis, particularly fetal TGF-II levels, without measurable anthropornetric changes at birth. Whether these effects have implications beyond the neonatal period remains to be determined. (c) 2006 Elsevier Ltd. All rights reserved.