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

被引:84
作者
Davis, EP
Townsend, EL
Gunnar, MR
Georgieff, MK
Guiang, SF
Ciffuentes, RF
Lussky, RC
机构
[1] Univ Calif Irvine, Dept Psychiat & Human Behav, Orange, CA 92868 USA
[2] Univ Minnesota, Inst Child Dev, Minneapolis, MN 55455 USA
[3] Univ Minnesota, Ctr Neurobehav Dev, Minneapolis, MN 55455 USA
[4] Univ Minnesota, Dept Pediat, Minneapolis, MN 55455 USA
[5] Hennepin Cty Med Ctr, Dept Pediat, Minneapolis, MN 55415 USA
关键词
cortisol; stress; HPA axis; prematurity; prenatal experience; betamethasone;
D O I
10.1016/j.psyneuen.2003.10.005
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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. (C) 2003 Elsevier Ltd. All rights reserved.
引用
收藏
页码:1028 / 1036
页数:9
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