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 Vol. 7 No. 3, March 2006
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NeoReviews Vol.7 No.3 2006 e135
© 2006 American Academy of Pediatrics

Fetal Adrenal Development

Implications For Lung Development and Postnatal Disease

Kristi Watterberg, MD*

* Professor of Pediatrics and Chief, Division of Neonatology, University of New Mexico School of Medicine, Albuquerque, NM

Abbreviations: AGA: appropriate for gestational age • BPD: bronchopulmonary dysplasia • CRH: corticotropin-releasing hormone • DHEA: dehydroepiandrosterone • DHEA-S: DHEA-sulfate • ELBW: extremely low birthweight • FIRS: fetal inflammatory response syndrome • HPA axis: hypothalamic-pituitary-adrenal axis • RDS: respiratory distress syndrome • SGA: small for gestational age • 11-beta-HSD2: 11-beta-hydroxysteroid dehydrogenase type 2 • 3-beta-HSD: 3-beta-hydroxysteroid dehydrogenase

The first 300 words of the full text of this article appear below.


   Objectives
 
After completing this article, readers should be able to:

  1. Describe the effects associated with increased glucocorticoid exposure during gestation.
  2. Describe the association of chorioamnionitis with acute respiratory distress and bronchopulmonary dysplasia in the preterm infant.
  3. List the conditions to which immaturity of the adrenal cortex may predispose preterm infants.


   Introduction
 
The adrenal glands undergo a remarkable metamorphosis during gestation and early postnatal life. The fetal glands grow exponentially, reaching a combined weight at term that equals the weight of the adult adrenal glands (about 8 g). This increase in weight is almost entirely due to hypertrophy of the "fetal zone" of the adrenal gland, which does not produce cortisol, but instead produces weak androgens (dehydroepiandrosterone [DHEA] and DHEA-sulfate [DHEAS]) that serve as precursors for placental estrogen production. Therefore, during normal gestation, fetal exposure to cortisol remains low until about 32 weeks, when fetal cortisol production begins to increase in preparation for extrauterine life (Fig. 1). After delivery, the adrenal glands involute rapidly as the fetal zone disappears, losing perhaps 75% of their weight in the first postnatal months before resuming growth at a much slower rate.


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  		Figure 1. Composite data for fetal cortisol concentrations during gestation compared with composite data reported in critically ill adults and data obtained from extremely low birthweight (ELBW) infants during the first and third weeks after birth. (1)

 
Fetal life is a time of rapid growth and cellular proliferation. Glucocorticoids, on the other hand, promote "maturation" (ie, cellular differentiation) (Fig. 2). Disruption of growth and proliferation by early exposure to excess glucocorticoid has both immediate and long-term growth-restricting effects and potentially alters the "fetal programming" that may affect future functioning of many organ systems. Animal studies have shown that fetuses exposed to abnormally high glucocorticoid concentrations are born with reduced brain, organ, and total . . . [Full Text of this Article]






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Copyright © 2006 by the American Academy of Pediatrics.