کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2803698 | 1156753 | 2006 | 9 صفحه PDF | دانلود رایگان |

ObjectiveWe examined the hypothesis that a single course of antenatal betamethasone influences the maternal–fetal insulin-IGF-GH axis.DesignA prospective, observational, pilot study consisting of four groups of pregnant women: (I) received betamethasone and delivered <2 weeks post treatment; (II) received betamethasone and delivered >2 weeks post treatment; (III) untreated women who delivered <37 weeks (preterm controls); (IV) 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.ResultsBetamethasone 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 or >2 weeks post betamethasone treatment. In Group IV, birth weight correlated positively with cord IGF-I levels (r2 = 0.41, p = 0.0098) and negatively with cord IGFBP-1 levels (r2 = 0.51, p = 0.0039), and ponderal index correlated negatively with cord IGFBP-1 levels (r2 = 0.27, p < 0.05).ConclusionsA single course of antenatal betamethasone influences the maternal–fetal insulin-IGF-GH axis, particularly fetal IGF-II levels, without measurable anthropometric changes at birth. Whether these effects have implications beyond the neonatal period remains to be determined.
Journal: Growth Hormone & IGF Research - Volume 16, Issue 4, August 2006, Pages 267–275