• Elysia Poggi Davis, Elise L Townsend, Megan R Gunnar, Michael K Georgieff, Sixto F Guiang, Raul F Ciffuentes, and Richard C Lussky.
• Department of Psychiatry and Human Behavior, University of California Irvine, City Tower, 333 City Boulevard West, Orange, CA 92868, USA. edavis@uci.edu
• Psychoneuroendocrinology. 2004 Sep 1; 29 (8): 1028-36.

AbstractThe 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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