Development of the Hypothalamic-Pituitary-Adrenal Axis in the Fetus and Preterm Infant

Bolt, R. J.; Weissenbruch, Mirjam M. van; Lafeber, Harry N; Waal, Henriëtte A. Delemarre-van de

doi:10.1515/jpem.2002.15.6.759

Cited by 37 publications

(31 citation statements)

References 83 publications

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“…In concordance with previous studies reviewed by Bolt et al [29], and Fernandez and Watterberg [9], we found relatively low cord F levels, which are probably maintained by the 11β-HSD type 2 enzyme converting maternally derived and fetally synthesized F to biologically inactive cortisone. At birth the contribution of placental progesterone to adrenal steroidogenesis stops and all F must be synthesized from cholesterol.…”

Section: Discussionsupporting

confidence: 93%

Serum Concentrations of Adrenal Steroids and Their Precursors as a Measure of Maturity of Adrenocortical Function in Very Premature Newborns

et al. 2010

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Background: Relative adrenocortical insufficiency is often seen in sick premature newborns. As the human fetal adrenal cortex does not express the 3β-hydroxysteroid dehydrogenase (3β-HSD) enzyme before about 23 weeks of gestation, we hypothesized that this enzymatic step may be rate limiting in cortisol synthesis in premature infants of less than 28 weeks postmenstrual age at birth. Methods: We measured cord, first day (D0) and median fourth day (D4) serum 17-OH-pregnenolone (17-OHPreg), 17-OH-progesterone (17-OHProg), 11-deoxycortisol, cortisol (F) and dehydroepiandrosterone sulphate concentrations and calculated the substrate/product ratios in 67 infants with gestational age 23.6–33.1 weeks. Results: The mean 17-OHPreg/17-OHProg ratio as a marker of 3β-HSD activity did not differ between the gestational age groups (gestational age <28 vs. ≧28 weeks: 0.40 vs. 0.48, p = 0.52 for cord, 3.1 vs. 2.4, p = 0.25 for D0, and 1.6 vs. 1.9, p = 0.62 for D4). In addition, the 17-OHPreg/17-OHProg ratio did not differ between the infants in the lowest F tertile compared to those in the highest F tertile group, and the serum 17-OHPreg and 17-OHProg concentrations were parallel with the respective F concentrations. Conclusion: We did not find evidence of significant immaturity in adrenal 3β-HSD activity in preterm infants between 24 and 28 weeks of gestation.

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Section: Discussionsupporting

confidence: 93%

Serum Concentrations of Adrenal Steroids and Their Precursors as a Measure of Maturity of Adrenocortical Function in Very Premature Newborns

et al. 2010

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“…The dampened cortisol response in the ELGA infants in the NICU may have occurred, at least in part, because preterm infants have varying degrees of immaturity in HPA axis function during the neonatal period (Bolt et al, 2000(Bolt et al, ,2002aKorte et al, 1996). In particular, infants born at lower gestational ages who are sickest commonly show low basal cortisol and adrenal insufficiency (e.g.…”

Section: Discussionmentioning

confidence: 99%

Neonatal procedural pain exposure predicts lower cortisol and behavioral reactivity in preterm infants in the NICU

Grunau

Holsti

Haley

et al. 2005

Pain

340

252

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Data from animal models indicate that neonatal stress or pain can permanently alter subsequent behavioral and/or physiological reactivity to stressors. However, cumulative effects of pain related to acute procedures in the neonatal intensive care unit (NICU) on later stress and/or pain reactivity has received limited attention. The objective of this study is to examine relationships between prior neonatal pain exposure (number of skin breaking procedures), and subsequent stress and pain reactivity in preterm infants in the NICU. Eighty-seven preterm infants were studied at 32 (±1 weeks) postconceptional age (PCA). Infants who received analgesia or sedation in the 72 h prior to each study, or any postnatal dexamethasone, were excluded. Outcomes were infant responses to two different stressors studied on separate days in a repeated measures randomized crossover design: (1) plasma cortisol to stress of a fixed series of nursing procedures; (2) behavioral (Neonatal Facial Coding System; NFCS) and cardiac reactivity to pain of blood collection. Among infants born ≤ 28 weeks gestational age (GA), but not 29-32 weeks GA, higher cumulative neonatal procedural pain exposure was related to lower cortisol response to stress and to lower facial (but not autonomic) reactivity to pain, at 32 weeks PCA, independent of early illness severity and morphine exposure since birth. Repeated neonatal procedural pain exposure among neurodevelopmentally immature preterm infants was associated with down-regulation of the hypothalamic-pituitary-adrenal axis, which was not counteracted with morphine. Differential effects of early pain on development of behavioral, physiologic and hormonal systems warrant further investigation.

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“…In humans, the HPA axis completes its maturation during the last trimester of pregnancy 284 (Bolt et al, 2002). In rats and mice, the critical development of this circuitry occurs 285 postnatally, during the first week of life (reviewed in (Rao, 2015)).…”

Section: Stress Circuitry 283mentioning

confidence: 99%

Hormonal and nutritional regulation of postnatal hypothalamic development

Sominsky

Jasoni

Twigg

et al. 2018

Journal of Endocrinology

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The hypothalamus is a key centre for regulation of vital physiological functions, such as appetite, stress responsiveness and reproduction. Development of the different hypothalamic nuclei and its major neuronal populations begins prenatally in both altricial and precocial species, with the fine tuning of neuronal connectivity and attainment of adult function established postnatally and maintained throughout adult life. The perinatal period is highly susceptible to environmental insults that, by disrupting critical developmental processes, can set the tone for the establishment of adult functionality. Here, we review the most recent knowledge regarding the major postnatal milestones in the development of metabolic, stress and reproductive hypothalamic circuitries, in the rodent, with a particular focus on perinatal programming of these circuitries by hormonal and nutritional influences. We also review the evidence for the continuous development of the hypothalamus in the adult brain, through changes in neurogenesis, synaptogenesis and epigenetic modifications. This degree of plasticity has encouraging implications for the ability of the hypothalamus to at least partially reverse the effects of perinatal mal-programming.

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Development of the Hypothalamic-Pituitary-Adrenal Axis in the Fetus and Preterm Infant

Cited by 37 publications

References 83 publications

Serum Concentrations of Adrenal Steroids and Their Precursors as a Measure of Maturity of Adrenocortical Function in Very Premature Newborns

Serum Concentrations of Adrenal Steroids and Their Precursors as a Measure of Maturity of Adrenocortical Function in Very Premature Newborns

Neonatal procedural pain exposure predicts lower cortisol and behavioral reactivity in preterm infants in the NICU

Hormonal and nutritional regulation of postnatal hypothalamic development

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