Effects of prenatal betamethasone exposure on regulation of stress physiology in healthy premature infants

Elysia Poggi Davis; Elise L. Townsend; Megan R. Gunnar; Michael K. Georgieff; Sixto F. Guiang; Raul F. Ciffuentes; Richard C. Lussky

doi:10.1016/j.psyneuen.2003.10.005

Effects of prenatal betamethasone exposure on regulation of stress physiology in healthy premature infants

Elysia Poggi Davis, Elise L. Townsend, Megan R. Gunnar, Michael K. Georgieff, Sixto F. Guiang, Raul F. Ciffuentes, Richard C. Lussky

Research output: Contribution to journal › Article › peer-review

95 Scopus citations

Abstract

The objective of this study was to examine the effects of prenatal exposure to betamethasone, a corticosteroid, on postnatal stress regulation, particularly activity of the hypothalamic-pituitary-adrenocortical (HPA) axis. Effects were assessed by measuring salivary cortisol production at baseline and in response to two potentially stressful events, a heel-stick blood draw and a physical exam, in infants born at 33-34 weeks gestation. Subjects included 9 infants with antenatal betamethasone treatment (2 doses of 12 mg of betamethasone administered intramuscularly to the mother twelve hours apart) and 9 infants without such treatment. Testing took place 3-6 days after delivery. Measures of behavioral distress confirmed that both events were stressful to these premature infants. Infants with betamethasone exposure, however, failed to exhibit increases in cortisol to either stressor. In contrast, infants without betamethasone exposure displayed elevated cortisol to the heel-stick blood draw but not the physical exam. These findings suggest that antenatal corticosteroids suppress infants' HPA response to a stressor typically encountered in a neonatal intensive care situation.

Original language	English (US)
Pages (from-to)	1028-1036
Number of pages	9
Journal	Psychoneuroendocrinology
Volume	29
Issue number	8
DOIs	https://doi.org/10.1016/j.psyneuen.2003.10.005
State	Published - Sep 2004

Bibliographical note

Funding Information:
This research was supported by grant from the Minnesota Medical Foundation (643-7051). The authors wish to give a very special thank you to the families who participated in this research and to the nurses, lab technicians, and physicians at Fairview University Medical Center and Hennepin County Medical Center, Minneapolis, MN. Thanks also to the many undergraduates at the University of Minnesota that assisted with data collection and to Andrea Geiben at the University of Trier for careful analysis of the salivary cortisol data.

Keywords

Betamethasone
Cortisol
HPA axis
Prematurity
Prenatal experience
Stress

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10.1016/j.psyneuen.2003.10.005

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title = "Effects of prenatal betamethasone exposure on regulation of stress physiology in healthy premature infants",

abstract = "The objective of this study was to examine the effects of prenatal exposure to betamethasone, a corticosteroid, on postnatal stress regulation, particularly activity of the hypothalamic-pituitary-adrenocortical (HPA) axis. Effects were assessed by measuring salivary cortisol production at baseline and in response to two potentially stressful events, a heel-stick blood draw and a physical exam, in infants born at 33-34 weeks gestation. Subjects included 9 infants with antenatal betamethasone treatment (2 doses of 12 mg of betamethasone administered intramuscularly to the mother twelve hours apart) and 9 infants without such treatment. Testing took place 3-6 days after delivery. Measures of behavioral distress confirmed that both events were stressful to these premature infants. Infants with betamethasone exposure, however, failed to exhibit increases in cortisol to either stressor. In contrast, infants without betamethasone exposure displayed elevated cortisol to the heel-stick blood draw but not the physical exam. These findings suggest that antenatal corticosteroids suppress infants' HPA response to a stressor typically encountered in a neonatal intensive care situation.",

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note = "Funding Information: This research was supported by grant from the Minnesota Medical Foundation (643-7051). The authors wish to give a very special thank you to the families who participated in this research and to the nurses, lab technicians, and physicians at Fairview University Medical Center and Hennepin County Medical Center, Minneapolis, MN. Thanks also to the many undergraduates at the University of Minnesota that assisted with data collection and to Andrea Geiben at the University of Trier for careful analysis of the salivary cortisol data. ",

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AU - Ciffuentes, Raul F.

AU - Lussky, Richard C.

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N2 - The objective of this study was to examine the effects of prenatal exposure to betamethasone, a corticosteroid, on postnatal stress regulation, particularly activity of the hypothalamic-pituitary-adrenocortical (HPA) axis. Effects were assessed by measuring salivary cortisol production at baseline and in response to two potentially stressful events, a heel-stick blood draw and a physical exam, in infants born at 33-34 weeks gestation. Subjects included 9 infants with antenatal betamethasone treatment (2 doses of 12 mg of betamethasone administered intramuscularly to the mother twelve hours apart) and 9 infants without such treatment. Testing took place 3-6 days after delivery. Measures of behavioral distress confirmed that both events were stressful to these premature infants. Infants with betamethasone exposure, however, failed to exhibit increases in cortisol to either stressor. In contrast, infants without betamethasone exposure displayed elevated cortisol to the heel-stick blood draw but not the physical exam. These findings suggest that antenatal corticosteroids suppress infants' HPA response to a stressor typically encountered in a neonatal intensive care situation.

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Effects of prenatal betamethasone exposure on regulation of stress physiology in healthy premature infants

Abstract

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Keywords

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