Changes in concentrations of cortisol, dehydroepiandrosterone sulphate and progesterone in fetal and maternal serum during pregnancy

Donaldson, A.; Nicolini, Umberto; Symes, Elizabeth K.; Rodeck, Charles H.; Tannirandorn, Yuen

doi:10.1111/j.1365-2265.1991.tb03564.x

Cited by 54 publications

(29 citation statements)

References 16 publications

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“…This process appears unaffected by preterm birth [21]. Fetal cortisol levels rise gradually from 20 weeks of gestation, then significantly from 32 to 41 weeks of gestation, whereas the fetal DHEAS concentration decreases linearly with gestation from 18 to 41 weeks [22], corresponding to the development and remodeling of the adrenal gland. This pattern of progression of fetal corticosteroid levels is important for fetal development to term.…”

Section: Adrenal and Thyroid Function In Extreme Prematuritymentioning

confidence: 91%

Hormonal Factors in the Morbidities Associated with Extreme Prematurity and the Potential Benefits of Hormonal Supplement

Yeung

Smyth²

2002

Neonatology

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Cortisol and thyroid hormones are known to modulate the maturation of various fetal organ systems, enzymes, and biochemical pathways. The cortisol furnished by the structural and biochemical immature fetal adrenal gland renders the extremely premature infants relatively cortisol deficient in comparison with the term newborns. The premature infants also have elevated fetal androgens, the production of which persists until ≈42 weeks of postconceptional age. The androgens produced by the fetal adrenal cortex and the müllerian inhibiting substance produced by the fetal testis have antiglucocorticoid and inhibitory effects on human fetal lung growth and maturation in vitro. Hypothalamic-pituitary-thyroid axis and thyroid function are also immature in extreme prematurity. In addition, there is reduced tissue thyroid hormone responsiveness. Superimposed on this is the reduced thyroid function seen in non-thyroidal illness in which elevated cytokine levels have been implicated. Repeated courses of antenatal steroids and high-dose postnatal dexamethasone appear to be deleterious to lung and brain development. This may be through inhibition of cell replication and catabolism as well as decreased thyroid-stimulating hormone secretion and reduced peripheral conversion of T₄ to T₃. Furthermore, dexamethasone has been found to enhance neurosteroid production in the immature brain, potentially altering brain development. Considered together, the relative cortisol deficiency/androgen excess and reduced thyroid function as well as prolonged high-dose postnatal dexamethasone therapy in these infants may be important factors in their high degree of morbidity. We propose to restrict antenatal steroids to a single course and hypothesize that the overall outcome of low-gestation infants would be improved with (1) hydrocortisone (i.v./p.o.) supplement at a fixed dose of 0.5 mg/kg birth weight every 12 h in infants <30 weeks of gestation from birth till 32 weeks of postconceptional age and (2) T₃ (i.v./p.o.) supplement at a fixed dose of 0.4 µg/kg birth weight every 12 h in those <27 weeks of gestation from birth till 32 weeks of postconceptional age.

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Section: Adrenal and Thyroid Function In Extreme Prematuritymentioning

confidence: 91%

Hormonal Factors in the Morbidities Associated with Extreme Prematurity and the Potential Benefits of Hormonal Supplement

Yeung

Smyth²

2002

Neonatology

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“…In mice, endogenous foetal plasma glucocorticoid levels increase rapidly from E15 (Michelsohn & Anderson 1992) though in humans this physiological increase happens in the week before birth (Fowden et al 1998). In addition, as pregnancy progresses into the final stage, maternal plasma glucocorticoid levels rise dramatically as a result of increased maternal glucocorticoid production and prolonged plasma half-life (Donaldson et al 1991, Mastorakos & Ilias 2003, though placental 11b-HSD2 restricts the access of maternal glucocorticoids to the foetus (Chapman et al 2013). Placental 11b-HSD2 activity declines in the last week of gestation in humans (Murphy & Clifton 2003) and in mice , Thompson et al 2002, allowing for transfer of maternal glucocorticoid to the foetus as birth approaches (Cottrell et al 2012).…”

Section: Figurementioning

confidence: 99%

Glucocorticoids and foetal heart maturation; implications for prematurity and foetal programming

Rog-Zielinska¹,

Richardson²,

Denvir³

et al. 2013

Journal of Molecular Endocrinology

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Glucocorticoids are steroid hormones, essential in mammals to prepare for life after birth. Blood levels of glucocorticoids (cortisol in most mammals including humans; corticosterone in rats and mice) rise dramatically shortly before birth. This is mimicked clinically in the routine administration of synthetic glucocorticoids to pregnant women threatened by a preterm birth or to preterm infants to improve neonatal survival. Whilst effects on lung are well documented and essential for postnatal survival, those on heart are less well known. In this study, we review recent evidence for a crucial role of glucocorticoids in late gestational heart maturation. Either insufficient or excessive glucocorticoid exposure before birth may alter the normal glucocorticoid-regulated trajectory of heart maturation with potential life-long consequences.

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“…Later in gestation, rising levels of 11b-HSD2 metabolize most of the maternal cortisol, releasing the fetal axis from suppression and resulting in increasing fetal cortisol production by the term infant. 23 In the extremely preterm infant, this suppression of the HPA axis by maternal cortisol likely contributes to the immaturity of the axis and possibly to relative adrenal insufficiency in the face of stress.…”

Section: Relative Adrenal Insufficiency In Critical Illnessmentioning

confidence: 99%

Relative adrenal insufficiency in the preterm and term infant

2009

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Cortisol release in the face of illness or stress is vital for survival. Relative adrenal insufficiency occurs when a patient's cortisol response is inadequate for the degree of illness or stress. Numerous studies have documented the existence of relative adrenal insufficiency in critically ill adults, and its association with increased morbidity and mortality. There is increasing evidence that relative adrenal insufficiency may be an etiology for hemodynamic instability and hypotension in the critically ill newborn, but compared with the adult population, there is still a paucity of data in this population. Randomized controlled trials are needed to evaluate the efficacy and safety of glucocorticoids for the treatment of cardiovascular insufficiency due to relative adrenal insufficiency in ill preterm and term newborn infants. Keywords: adrenocorticotropin; ACTH; adrenal insufficiency; corticotrophin-releasing hormone; cortisol; critically ill infants hypothalamic-pituitary-adrenal axis; newborns-full term Introduction Activation of the hypothalamic-pituitary-adrenal (HPA) axis and ultimate release of cortisol are critical in maintaining homeostasis in response to stress. Relative adrenal insufficiency occurs when the HPA axis produces insufficient cortisol for the degree of illness or stress. In some critically ill adult populations, relative adrenal insufficiency is prevalent, 1-4 and is associated with increased morbidity and mortality. 2,3,5 Some studies of glucocorticoid treatment in critically ill adults have shown benefit, with faster reversal of shock and reduction in mortality. 3,[5][6][7][8] Recently, increasing evidence supports the existence of relative adrenal insufficiency in ill newborns, but, similar to other ill populations, there remains no general consensus on which patients should be tested, which tests to use and how to interpret them, which patients should be treated or how they should be treated. 9 The following discussion is an overview of corticosteroid physiology, relative adrenal insufficiency in critically ill populations and evidence of its existence in newborn infants, with proposed underlying

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Changes in concentrations of cortisol, dehydroepiandrosterone sulphate and progesterone in fetal and maternal serum during pregnancy

Abstract: These results are compatible with the proposed role of cortisol in fetal lung maturation, confirm high levels of progesterone in the fetus from an early stage of gestation, and provide further evidence for placental progesterone being the precursor of fetal cortisol.

Cited by 54 publications

References 16 publications

Hormonal Factors in the Morbidities Associated with Extreme Prematurity and the Potential Benefits of Hormonal Supplement

Hormonal Factors in the Morbidities Associated with Extreme Prematurity and the Potential Benefits of Hormonal Supplement

Glucocorticoids and foetal heart maturation; implications for prematurity and foetal programming

Relative adrenal insufficiency in the preterm and term infant

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