Neuroendocrine regulation of pituitary–adrenal function during fetal life

An, Bo; Hagan, DM; Howe, DC

doi:10.1530/eje.0.1350153

Cited by 26 publications

(12 citation statements)

References 107 publications

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“…An increase in cortisol secretion in late gestation is required for lung maturation. Specific developmental changes such as alveolar septal thinning, surfactant synthesis, and maturation of the pulmonary capillary system have been associated with increases in fetal cortisol levels [24] . Additionally, supplemental dexamethasone was shown to significantly downregulate Hoxb-5 expression in cultured murine fetal lungs [25] .…”

Section: Discussionmentioning

confidence: 99%

Effect of Maternal Betamethasone Administration on Prenatal Congenital Cystic Adenomatoid Malformation Growth and Fetal Survival

et al. 2007

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Objective: To evaluate the effect of prenatal steroid treatment on the growth of congenital cystic adenomatoid malformations (CCAM) and survival in affected fetuses not amenable to other percutaneous ultrasound-guided prenatal interventions. Methods: A retrospective review of patients with a CCAM or hybrid lesion treated with two maternal prenatal betamethasone injections was performed. Patients receiving cyst aspiration or thoracoamniotic shunting at the time of or after steroid administration were excluded. Growth rates and survival data were compared to historical non-steroid treated controls. Results: Eleven patients were treated with prenatal steroids (10 microcystic and 1 macrocystic). Survival was 100% in fetuses with hydrops (5/5) or a CCAM volume ratio (CVR) >1.6 (7/7) at the time of steroid administration. This compares to a mortality of 100 and 56.2% respectively in historical non-treated controls. Resolution of hydrops was seen in 80% (4/5) of steroid-treated patients. CCAM growth rates were variable after steroid administration. However, when compared to historical data where CVR and CCAM volume have been documented to increase until 28 weeks’ gestation, the CVR and CCAM volume growth rates decreased in 72.73% and 50% of patients respectively from the time of steroid administration to 28 weeks’ gestation. Conclusions: In the fetus with a CCAM, the presence of hydrops fetalis or a CVR >1.6 is indicative of poor fetal outcome without prenatal intervention. The observed effect of antenatal steroid treatment on CCAM growth is variable, but its potential to improve survival in these high-risk groups is encouraging and warrants further controlled evaluations.

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Section: Discussionmentioning

confidence: 99%

Effect of Maternal Betamethasone Administration on Prenatal Congenital Cystic Adenomatoid Malformation Growth and Fetal Survival

et al. 2007

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“…Infusion of PGE 2 into catheterized fetal sheep resulted in a significant elevation in circulating ACTH and cortisol concentrations [156,157]. Placental PGE 2 may represent a unique positive feed-forward mechanism whereby an increase in fetal glucocorticoids stimulates placental prostaglandin (PG) production and PGs further stimulate an increase in fetal HPA activity [159]. Placental PGE 2 may represent a unique positive feed-forward mechanism whereby an increase in fetal glucocorticoids stimulates placental prostaglandin (PG) production and PGs further stimulate an increase in fetal HPA activity [159].…”

Section: Placental Effectsmentioning

confidence: 99%

Synthetic Glucocorticoids: Antenatal Administration and Long-term Implications

Sloboda¹,

Challis

Moss³

et al. 2005

CPD

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A clear relationship between intrauterine development and later life predisposition to long-term disease is well established. Weight at birth provides a surrogate measure for fetal development and low birth weight predicts changes in most endocrine axes in adulthood. The exposure of the fetus to elevated levels of either endogenous or synthetic glucocorticoids, pre and periconceptional nutritional status and immediate postnatal development including catch-up growth all contribute substantially to the development of adult onset disease. Fetal exposure to high levels of glucocorticoids has direct clinical relevance. Synthetic glucocorticoids (betamethasone/ dexamethasone) are administered to women at risk of preterm delivery to advance fetal maturation and reduce neonatal morbidity and mortality. However, in human pregnancy, evidence suggests that fetal exposure to synthetic glucocorticoids has detrimental effects on birth outcome, childhood cognition and long-term behavior. Studies in animals have established a link between prenatal exposure to synthetic glucocorticoids and alterations in fetal development as well as changes in placental function. These developmental alterations appear to be permanent. Whether this is the case in humans awaits long-term follow-up of children enrolled in randomized controlled trials of prenatal glucocorticoid therapy. The research challenges in this field are now centered on uncovering the mechanisms by which glucocorticoids are involved in programming the fetus for its future life, and discovering ways in which the effectiveness and safety of antenatal glucocorticoids can be enhanced. The purpose of this mini-review is to provide a background into the use of antenatal synthetic corticosteroids and to highlight and summarize recently published clinical and animal-based studies.

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“…During fetal development, there is a progressive increase in plasma concentrations of cortisol in the last 15-20 days of gestation and a dramatic surge in the final few days before birth (11).…”

Section: Introductionmentioning

confidence: 99%

IGF-I and IGF-binding protein-1 are related to cortisol in human cord blood

Cianfarani

Germani

Rossi³

et al. 1998

European Journal of Endocrinology

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Objective: To assess cortisol concentrations in cord blood and investigate their relationships with the IGF system. Study design: Fifteen newborns with birth weight appropriate for gestational age (AGA) and 30 children with intrauterine growth retardation (IUGR) were studied. Serum samples were collected from umbilical cord blood and cortisol, IGF-I and IGF-binding proteins (IGFBPs)-1 and -3 were measured. IUGR infants were followed up for 3 months with repeated measurements of weight, supine length and knee-heel length (by knemometry). Results: IUGR newborns showed significantly greater concentrations of IGFBP-1 (P<0·0001) and lower concentrations of IGF-I (P < 0.0001) and IGFBP-3 (P < 0.0001) than did controls. In AGA children, cortisol correlated inversely with IGF-I (r ¼ ¹0.75, P < 0.002) and directly with IGFBP-1 (r ¼ 0.52, P < 0·05), whereas no correlation between cortisol and IGF system-related variables was observed in IUGR. Finally, in IUGR children an inverse correlation was found between length gain in the first trimester of life and cortisol concentrations at birth (r ¼ ¹0.54, P < 0.005). Conclusions: Cortisol might be a physiological regulator of fetal growth, at least in the last part of pregnancy, by modulating IGF-I and IGFBP-1 release under conditions of fetal stress. In IUGR children, a rearrangement of this growth control mechanism seems to occur. The close inverse relationship of cortisol with linear growth, if confirmed by large-scale studies, suggests cord blood cortisol to be potentially predictive of early postnatal catch-up growth in IUGR infants.

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Neuroendocrine regulation of pituitary–adrenal function during fetal life

Cited by 26 publications

References 107 publications

Effect of Maternal Betamethasone Administration on Prenatal Congenital Cystic Adenomatoid Malformation Growth and Fetal Survival

Effect of Maternal Betamethasone Administration on Prenatal Congenital Cystic Adenomatoid Malformation Growth and Fetal Survival

Synthetic Glucocorticoids: Antenatal Administration and Long-term Implications

IGF-I and IGF-binding protein-1 are related to cortisol in human cord blood

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