The Regulation and Role of Fetal Adrenal Development in Human Pregnancy

Jaffe, Robert B.; Mesiano, Sam; Smith, Roger; Coulter, Catherine; Spencer, Susan J.; Chakravorty, Aruna

doi:10.3109/07435809809032707

Cited by 33 publications

(11 citation statements)

References 19 publications

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“…These findings suggest that the human adrenal function is not yet fully matured in preterm infants and indicates a decreased capacity for cortisol synthesis and/or a decreased responsiveness to ACTH (15). This may be related to a gradual maturation of the human fetal HPA axis during the third trimester of gestation and is in agreement with the work of Mesiano and Jaffe in primates (16,17). No differences were found in levels of 17-OHP between infants born before 30 wk and infants born after 30 wk.…”

Section: Discussionsupporting

confidence: 81%

Maturity of the Adrenal Cortex in Very Preterm Infants Is Related to Gestational Age

Bolt

2002

Pediatric Research

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To study the maturity of the adrenal cortex in preterms born before 33 wk of gestation, basal levels of cortisol and cortisone and the cortisol and 17-hydroxyprogesterone (17-OHP) response to 1 g/kg adrenocorticotropic hormone stimulation were measured in 24 appropriate-for-gestational age preterm infants (26-33 wk; 690-1985 g). Gestational age influenced the response of cortisol, 17-OHP, and the ratio between cortisol/17-OHP in the studied infants. In preterms born Ͻ30 wk of gestation, levels of cortisol, and the ratio between cortisol/17-OHP were lower compared with preterms born between 30 and 33 wk. Levels of cortisone were higher in preterms born Ͻ30 wk, suggesting a lower activity of 11␤-hydroxysteroid dehydrogenase that may be related to maturity as well. The adrenal gland plays an important role during gestation. Steroid hormones produced by the fetal adrenal cortex are involved in the maturation of organ systems necessary for intrauterine and extrauterine life. For example, secretion of cortisol in late gestation is essential for lung maturation in sheep, rats, monkeys, and possibly humans (1, 2). It has been suggested that the adrenal cortex function may be more closely related to gestational age rather than to birth (3, 4), which implicates that in very preterm infants the adrenal activity may still be immature. Immaturity of the hypothalamic-pituitaryadrenal (HPA)-axis in preterm infants has been suggested to be associated with the occurrence of respiratory distress syndrome, chronic lung disease of prematurity, or even cardiovascular instability (5-7). Therefore, the ability of the HPA-axis to regulate, synthesize, and secrete cortisol in response to stress may be critical for survival and pulmonary development in very preterm infants.To evaluate the adrenal function the plasma cortisol response to i.v. administered ACTH is a common screening test. In general, 250 g synthetic ACTH is given as a bolus dose to stimulate cortisol release from the adrenal cortex, in adults as well as children as described by Wood et al. in 1965 (8). This supra-physiologic dose is much higher than required to produce a maximal adrenal response and could elicit an appropriate response despite of adrenal insufficiency (9, 10). Therefore, a lower dose of ACTH has been proposed to study the adrenal function.We hypothesize that differences in the maturity of the HPAaxis related to gestational age can be observed in the levels of hormones produced by the adrenal cortex and the adrenal response to ACTH in preterm infants of different gestational ages. The objective was to study basal levels of glucocorticoids and to establish the effect of stimulation of the adrenal cortex with ACTH in very preterm infants at the end of the 1st week of life. PATIENTS AND METHODS Patients.The study group consisted of 24 preterm infants with gestational ages ranging from 26 to 33 wk and birth weights ranging from 690 to 1985 g. Patients admitted to our July 11, 2001; January 10, 2002

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Section: Discussionsupporting

confidence: 81%

Maturity of the Adrenal Cortex in Very Preterm Infants Is Related to Gestational Age

Bolt

2002

Pediatric Research

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“…Fetal DHEAS is produced in the fetal zone of the adrenal gland and provides a basic substrate for estrogen synthesis by the placenta [27,28]. Because placental estrogen synthesis increases with advancing gestation, a decrease in DHEAS at this stage is unexpected.…”

Section: Discussionmentioning

confidence: 95%

Fetal plasma cortisol and dehydroepiandrosterone sulfate concentrations in pregnancy and term parturition

Romero

Shim

et al. 2006

The Journal of Maternal-Fetal & Neonatal Medicine

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(1) Fetal plasma cortisol remained unchanged until 36 weeks of gestation and increased thereafter to term; (2) active labor was associated with a significant increase in fetal plasma cortisol; (3) fetal plasma DHEAS increased at term gestation (>36 weeks) but did not increase during active labor; (4) the cortisol/DHEAS ratio (stress index) increased with advancing gestation and with active labor at term. CONCLUSIONS. Human parturition at term is associated with an increase in fetal plasma cortisol and in the cortisol/DHEAS ratio, but not in DHEAS.

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“…It is possible that the increasing production of cortisol by the maturing fetal adrenal induces placental CRF expression [80]. Placenta-derived CRFas well as UCN1 stimulate the production of DHEAS by the fetal zone of human adrenals via the CRF 1 receptor, which is expressed in the fetal zone [81][82][83]. Indeed, CRF induces the transcription of cytochrome P450 cholesterol side-chain cleavage and 17a-hydroxylase/ 17,20 lyase in fetal adrenal cells.…”

Section: Modes Of Crf Action On the Adrenalsmentioning

confidence: 95%

The corticotropin-releasing factor (CRF) family of peptides as local modulators of adrenal function

Tsatsanis

Dermitzaki

Venihaki

et al. 2007

Cell. Mol. Life Sci.

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Corticotropin-releasing factor (CRF), also termed corticotropin-releasing hormone (CRH) or corticoliberin, is the major regulator of the adaptive response to internal or external stresses. An essential component of the adaptation mechanism is the adrenal gland. CRF regulates adrenal function indirectly through the central nervous system (CNS) via the hypothalamic-pituitary-adrenal (HPA) axis and via the autonomic nervous system by way of locus coeruleus (LC) in the brain stem. Accumulating evidence suggests that CRF and its related peptides also affect the adrenals directly, i.e. not through the CNS but from within the adrenal gland where they form paracrine regulatory loops. Indeed, CRF and its related peptides, the urocortins (UCNs: UCN1, UCN2 and UCN3), their receptors CRF type 1 (CRF(1)) and 2 (CRF(2)) as well as the endogenous pseudo-receptor CRF-binding protein (CRF-BP) are all expressed in adrenal cortical, medullary chromaffin and resident immune cells. The intra-adrenal CRF-based regulatory system is complex and depends on the balance between the local concentration of CRF ligands and the availability of their receptors.

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The Regulation and Role of Fetal Adrenal Development in Human Pregnancy

Cited by 33 publications

References 19 publications

Maturity of the Adrenal Cortex in Very Preterm Infants Is Related to Gestational Age

Maturity of the Adrenal Cortex in Very Preterm Infants Is Related to Gestational Age

Fetal plasma cortisol and dehydroepiandrosterone sulfate concentrations in pregnancy and term parturition

The corticotropin-releasing factor (CRF) family of peptides as local modulators of adrenal function

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