Accelerated lung maturation following maternal steroid treatment in infants born before 30 weeks gestation

Kattner, E.; Metze, Boris; E, Waiss; Obladen, Michael

doi:10.1515/jpme.1992.20.6.449

Cited by 33 publications

(19 citation statements)

References 33 publications

(22 reference statements)

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“…The HPA axis is particularly susceptible to early life programming and will alter the negative feedback mechanisms. Prenatal treatment with glucocorticoids is a clinical procedure used to induce lung maturation in anticipated preterm delivery (Kattner et al, 1992). It has been found that prenatal exposure to glucocorticoids can not only have deleterious effects on fetal growth and metabolism but that these effects can extend into adult life.…”

Section: Prenatal Treatment With Glucocorticoidsmentioning

confidence: 99%

Protecting the auditory system with glucocorticoids

Meltser

Canlon

2011

Hearing Research

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Section: Prenatal Treatment With Glucocorticoidsmentioning

confidence: 99%

Protecting the auditory system with glucocorticoids

Meltser

Canlon

2011

Hearing Research

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“…Glucocorticoids are used as immunosuppressants to control various maternal conditions, such as connective tissue disorders [130], and are used extensively in obstetric practice, primarily to accelerate lung maturation in cases of threatened preterm labour [131], which may occur in up to 10 % of pregnancies. There is no doubt that such synthetic glucocorticoids enhance lung maturation and reduce mortality in preterm infants [132].…”

Section: Evidence For Glucocorticoid Programming In Humansmentioning

confidence: 99%

Mechanisms underlying the role of glucocorticoids in the early life programming of adult disease

2007

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Compelling epidemiological evidence suggests that exposure to an adverse intrauterine environment, manifested by low-birth weight, is associated with cardiometabolic and behavioural disorders in adulthood. These observations have led to the concept of 'fetal programming'. The molecular mechanisms that underlie this relationship remain unclear, but are being extensively investigated using a number of experimental models. One major hypothesis for early life physiological programming implicates fetal overexposure to stress (glucocorticoid) hormones. Several animal studies have shown that prenatal glucocorticoid excess, either from endogenous overproduction with maternal stress or through exogenous administration to the mother or fetus, reduces birth weight and causes lifelong hypertension, hyperglycaemia and behavioural abnormality in the offspring. Intriguingly, these effects are transmitted across generations without further exposure to glucocorticoids, which suggests an epigenetic mechanism. These animal observations could have huge implications if extrapolated to humans, where glucocorticoids have extensive therapeutic use in obstetric and neonatal practice.

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“…Dexamethasone (DEX), a synthetic GC (sGC), is administered in ϳ10% of human pregnancies (32) due to its effectiveness in suppressing uterine contractions and promoting lung maturation (21,35). However, studies in rat models have shown that DEX exposure in utero may give rise to adverse effects in adulthood.…”

mentioning

confidence: 99%

Prenatal exposure to dexamethasone alters hippocampal drive on hypothalamic-pituitary-adrenal axis activity in adult male rats

Shoener¹,

Baig²,

Page³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

101

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Glucocorticoids are essential for normal hypothalamic-pituitary-adrenal (HPA) axis activity; however, recent studies warn that exposure to excess endogenous or synthetic glucocorticoid during a specific period of prenatal development adversely affects HPA axis stability. We administered dexamethasone (DEX) to pregnant rats during the last week of gestation and investigated subsequent HPA axis regulation in adult male offspring in unrestrained and restraint-stressed conditions. With the use of real-time PCR and RIA, we examined the expression of regulatory genes in the hippocampus, hypothalamus, and pituitary, including corticotropin-releasing hormone (CRH), arginine vasopressin (AVP), glucocorticoid receptors (GR), mineralcorticoid receptors (MR), and 11-␤-hydroxysteroid dehydrogenase-1 (11␤-HSD-1), as well as the main HPA axis hormones, adrenal corticotropic hormone (ACTH) and corticosterone (CORT). Our results demonstrate that the DEX-exposed group exhibited an overall change in the pattern of gene expression and hormone levels in the unrestrained animals. These changes included an upregulation of CRH in the hypothalamus, a downregulation of MR with a concomitant upregulation of 11␤-HSD-1 in the hippocampus, and an increase in circulating levels of both ACTH and CORT relative to unrestrained control animals. Interestingly, both DEX-exposed and control rats exhibited an increase in pituitary GR mRNA levels following a 1-h recovery from restraint stress; however, the increased expression in DEX-exposed rats was significantly less and was associated with a slower return to baseline CORT compared with controls. In addition, circulating levels of ACTH and CORT as well as hypothalamic CRH and hippocampal 11␤-HSD-1 expression levels were significantly higher in the DEX-exposed group compared with controls following restraint stress. Taken together, these data demonstrate that late-gestation DEX exposure in rats is associated with persistent changes in both the modulation of HPA axis activity and the HPA axis-mediated response to stress. mineralcorticoid receptor:glucocorticoid receptor balance; 11-␤-hydroxysteroid dehydrogenase-1; circadian rhythm; restraint stress A CONSIDERABLE BODY OF EVIDENCE indicates that the limbic system is a central modulator of hypothalamic-pituitary-adrenal (HPA) axis activity (18,41) and that it is exquisitely sensitive to fluctuations in circulating corticosteroids (27,28,56). Corticosteroid receptors, which include both mineralcorticoid receptors (MR) and glucocorticoid receptors (GR), are highly expressed in this system (29,44) and are colocalized in distinct regions, particularly the hippocampus (51, 53). In contrast, nonlimbic sites, such as the prefrontal cortex, hypothalamus, and pituitary, express predominantly GR (10, 43).

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Accelerated lung maturation following maternal steroid treatment in infants born before 30 weeks gestation

Cited by 33 publications

References 33 publications

Protecting the auditory system with glucocorticoids

Protecting the auditory system with glucocorticoids

Mechanisms underlying the role of glucocorticoids in the early life programming of adult disease

Prenatal exposure to dexamethasone alters hippocampal drive on hypothalamic-pituitary-adrenal axis activity in adult male rats

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