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Abstract

To the Editors:Numerous investigators have reported that maternal glucocorticoid treatments routinely cause fetal growth restriction in rodents and rabbits. High or prolonged fetal exposure of primates to glucocorticoids also results in fetal growth restriction. The goals of our study were to evaluate with the use of pregnant sheep the effects of maternal glucocorticoid treatments that are consistent with current clinical practice. Maternal betamethasone caused proportionate fetal growth restriction after preterm or term delivery and after single or repetitive exposures at 7-day intervals. We did not evaluate maternal weights after the betamethasone treatments, but we doubt that a single maternal dose of betamethasone would change maternal weight 40 days after treatment. We have subsequently found that direct fetal treatments with betamethasone does not cause fetal growth restriction but does induce lung maturation.1Jobe AH Newnham J Willet K Sly P Ikegami M Single and repetitive doses of maternal antenatal betamethasone (beta) are more potent than fetal beta [abstract].Pediatr Res. 1998; 43: 178ACrossref PubMed Google Scholar Fetal plasma glucocorticoid levels are higher after fetal than after maternal treatment.2Berry LM Polk DH Ikegami M Jobe AH Padbury JF Ervin MG Preterm newborn lamb renal and cardiovascular responses after fetal or maternal antenatal betamethasone.Am J Physiol. 1997; 272: R1972-R1979PubMed Google Scholar These observations suggest that the growth restriction resulting from maternal glucocorticoid exposure does not result directly from the glucocorticoid. Although fetal growth inhibition by antenatal glucocorticoids has been known for >40 years, as pointed out by Kalter, the mechanisms responsible for the fetal growth and maturation effects remain to be characterized. To the Editors:Numerous investigators have reported that maternal glucocorticoid treatments routinely cause fetal growth restriction in rodents and rabbits. High or prolonged fetal exposure of primates to glucocorticoids also results in fetal growth restriction. The goals of our study were to evaluate with the use of pregnant sheep the effects of maternal glucocorticoid treatments that are consistent with current clinical practice. Maternal betamethasone caused proportionate fetal growth restriction after preterm or term delivery and after single or repetitive exposures at 7-day intervals. We did not evaluate maternal weights after the betamethasone treatments, but we doubt that a single maternal dose of betamethasone would change maternal weight 40 days after treatment. We have subsequently found that direct fetal treatments with betamethasone does not cause fetal growth restriction but does induce lung maturation.1Jobe AH Newnham J Willet K Sly P Ikegami M Single and repetitive doses of maternal antenatal betamethasone (beta) are more potent than fetal beta [abstract].Pediatr Res. 1998; 43: 178ACrossref PubMed Google Scholar Fetal plasma glucocorticoid levels are higher after fetal than after maternal treatment.2Berry LM Polk DH Ikegami M Jobe AH Padbury JF Ervin MG Preterm newborn lamb renal and cardiovascular responses after fetal or maternal antenatal betamethasone.Am J Physiol. 1997; 272: R1972-R1979PubMed Google Scholar These observations suggest that the growth restriction resulting from maternal glucocorticoid exposure does not result directly from the glucocorticoid. Although fetal growth inhibition by antenatal glucocorticoids has been known for >40 years, as pointed out by Kalter, the mechanisms responsible for the fetal growth and maturation effects remain to be characterized. Numerous investigators have reported that maternal glucocorticoid treatments routinely cause fetal growth restriction in rodents and rabbits. High or prolonged fetal exposure of primates to glucocorticoids also results in fetal growth restriction. The goals of our study were to evaluate with the use of pregnant sheep the effects of maternal glucocorticoid treatments that are consistent with current clinical practice. Maternal betamethasone caused proportionate fetal growth restriction after preterm or term delivery and after single or repetitive exposures at 7-day intervals. We did not evaluate maternal weights after the betamethasone treatments, but we doubt that a single maternal dose of betamethasone would change maternal weight 40 days after treatment. We have subsequently found that direct fetal treatments with betamethasone does not cause fetal growth restriction but does induce lung maturation.1Jobe AH Newnham J Willet K Sly P Ikegami M Single and repetitive doses of maternal antenatal betamethasone (beta) are more potent than fetal beta [abstract].Pediatr Res. 1998; 43: 178ACrossref PubMed Google Scholar Fetal plasma glucocorticoid levels are higher after fetal than after maternal treatment.2Berry LM Polk DH Ikegami M Jobe AH Padbury JF Ervin MG Preterm newborn lamb renal and cardiovascular responses after fetal or maternal antenatal betamethasone.Am J Physiol. 1997; 272: R1972-R1979PubMed Google Scholar These observations suggest that the growth restriction resulting from maternal glucocorticoid exposure does not result directly from the glucocorticoid. Although fetal growth inhibition by antenatal glucocorticoids has been known for >40 years, as pointed out by Kalter, the mechanisms responsible for the fetal growth and maturation effects remain to be characterized.