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: 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, 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 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).Conclusions. A 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.Irfan Ahmad, MD 1 Running Title: Betamethasone and the insulin-IGF-GH axis. INFLUENCE OF A SINGLE COURSE OF ANTENATAL BETAMETHASONE ON THE MATERNAL-FETAL INSULIN-IGF-GH AXIS IN SINGLETON PREGNANCIES * ManuscriptIrfan Ahmad, MD 2 ABSTRACTObjective. 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: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, GHBP. Results. Betamethasone increased maternal insulin, glucose and IGF-I levels without affectingIGFBPs. 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 (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...

Idiopathic cerebral infarction is very rare in neonates and has been described as being associated with upper extremity ischemia in a handful of cases. We report on two cases in which no etiology was found and review the literature on this interesting entity.

Ascorbic acid (AA) is a powerful antioxidant required for the defense against oxidative stress. At present it is not known whether AA may play a role in the developmental process of the fetus. We therefore determined the relationship of AA levels between the umbilical cord vein (UCV) and umbilical cord artery (UCA) of preterm (< 37 weeks of gestation) and term (> 37 weeks of gestation) infants and compared those levels to matched maternal venous AA levels. We also assessed the association between UCV plasma AA levels with birth weight and gestational age by measuring AA in 88 UCV plasma samples and 58 UCA plasma samples obtained from newborn infants ranging in gestational age from 24 to 42 weeks and birth weight from 675 to 5,020 g, by high pressure liquid chromatography. Maternal venous samples were collected at the time of delivery. The mean UCV plasma AA levels (mg/dl) were significantly lower in the preterm group than in the term group (0.43 ± 0.59 and 1.16 ± 0.97, respectively; p < 0.002); however, the mean UCA plasma AA levels did not differ between the groups. In contrast, mean maternal venous plasma AA levels of the preterm group (1.33 ± 0.62) were significantly higher than those of the mothers in the term group (0.72 ± 0.69; p < 0.01). A direct correlation was found between UCV levels and birth weight (r = 0.23, p < 0.05), and UCV levels and gestational age (r = 0.23, p < 0.05). We speculate that the preterm gestation, AA may be transported across the placenta in its oxidized form (dehydroascorbic acid) to the fetus, where it is then reduced to AA. The underlying mechanism(s) involved in this process and the clinical significance of these findings need to be elucidated.

We conclude that elevated MMP-2 activity in the maternal and fetoplacental compartments may suggest a mechanism, in part, for betamethasone-induced fetal lung maturation.

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