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This Article Full Text Full Text (PDF) All Versions of this Article: 297/2/R510    most recent 00175.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Stark, M. J. Articles by Clifton, V. L. PubMed PubMed Citation Articles by Stark, M. J. Articles by Clifton, V. L.

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Sex-specific alterations in placental 11β-hydroxysteroid dehydrogenase 2 activity and early postnatal clinical course following antenatal betamethasone

¹The Robinson Institute, Department of Paediatrics and Reproductive Health, University of Adelaide, South Australia, Australia, ²Mothers and Babies Research Centre, University of Newcastle and The Kaleidoscope Neonatal Intensive Care Unit, John Hunter Children's Hospital, Newcastle, New South Wales, Australia

Submitted 25 March 2009 ; accepted in final form 11 June 2009

Placental 11β-hydroxysteroid dehydrogenase-2 (11βHSD2) limits fetal glucocorticoid exposure and is associated with physiological stability in the premature newborn infant. Antenatal betamethasone alters 11βHSD2 activity and confers sex-specific advantages in neonatal outcome. We investigated the influence of betamethasone and sex on 11βHSD2 activity, neonatal adrenal function and clinical course in 24- to 36-wk gestation neonates from birth to day 5 of life. Univariate analyses demonstrated an interaction between timing of betamethasone exposure and sex for 11βHSD2 activity rate (P = 0.02) and umbilical arterial cortisol (P = 0.01). For infants born < 72 h following antenatal betamethasone, females had higher 11βHSD2 activity (P < 0.01) and umbilical arterial cortisol (P = 0.01) than males. Females born < 72 h of betamethasone exposure had higher day 1 urinary cortisol, if exposed to perinatal stress, than males (P < 0.01). For infants born < 72 h after betamethasone exposure, 11βHSD2 activity was negatively correlated with Clinical Illness Severity Score score (r = –0.79 P = 0.01) and positively correlated with mean arterial blood pressure (r = 0.8 P = 0.01) only in females. Sex-specific placental 11BHSD2 autoregulation following antenatal betamethasone exposure may limit adrenal suppression in females influencing physiological stability following preterm birth. A lack of adjustment in 11βHSD2 and adrenal response may contribute to the increased incidence of poor outcome observed in preterm males.

placenta; fetal sex