Fetal development is a critical period for shaping the lifelong health of an individual. However, the fetus is susceptible to internal and external stimuli that can lead to adverse long-term health consequences. Glucocorticoids are an important developmental switch, driving changes in gene regulation that are necessary for normal growth and maturation. The fetal hypothalamic-pituitary-adrenal (HPA) axis is particularly susceptible to long-term programming by glucocorticoids; these effects can persist throughout the life of an organism. Dysfunction of the HPA axis as a result of fetal programming has been associated with impaired brain growth, altered behaviour and increased susceptibility to chronic disease (such as metabolic and cardiovascular disease). Moreover, the effects of glucocorticoid-mediated programming are evident in subsequent generations, and transmission of these changes can occur through both maternal and paternal lineages.

Glucocorticoids and fetal programming part 1: Outcomes.

Pregnancy dramatically affects the hypothalamic-pituitary-adrenal axis leading to increased circulating cortisol and ACTH levels during gestation, reaching values in the range seen in Cushing's syndrome (CS). The cause(s) of increased ACTH may include placental synthesis and release of biologically active CRH and ACTH, pituitary desensitization to cortisol feedback, or enhanced pituitary responses to corticotropin-releasing factors. In this context, challenges in diagnosis and management of disorders of the hypothalamic-pituitary-adrenal axis in pregnancy are discussed. CS in pregnancy is uncommon and is associated with fetal morbidity and mortality. The diagnosis may be missed because of overlapping clinical and biochemical features in pregnancy. The proportion of patients with primary adrenal causes of CS is increased in pregnancy. CRH stimulation testing and inferior petrosal sinus sampling can identify patients with Cushing's disease. Surgery is a safe option for treatment in the second trimester; otherwise medical therapy may be used. Women with known adrenal insufficiency that is appropriately treated can expect to have uneventful pregnancies. Whereas a fetal/placental source of cortisol may mitigate crisis during gestation, unrecognized adrenal insufficiency may lead to maternal or fetal demise either during gestation or in the puerperium. Appropriate treatment and management of labor are reviewed.

/pdf/the-hypothalamic-pituitary-adrenal-axis-in-pregnancy-4xacp189q5.pdf

The Hypothalamic-Pituitary-Adrenal Axis in Pregnancy: Challenges in Disease Detection and Treatment

https://escholarship.org/content/qt0fx6q4k8/qt0fx6q4k8.pdf?t=pqtpll

Elevated maternal cortisol early in pregnancy predicts third trimester levels of placental corticotropin releasing hormone (CRH): priming the placental clock.

The human fetal adrenal cortex, a pivotal member of the feto-placental unit, is a relatively large organ with steroidogenic activity that is spatially, temporally and functionally regulated. The present review aims to identify what we know and what we need to know about the developmental processes, functional aspects, and physiologic significance of this unique organ.

Development and function of the human fetal adrenal cortex: a key component in the feto-placental unit.

Increased CRH secretion by the placenta of pregnant women has been associated with preterm birth. Certain indices of risk, both medical and psychosocial in nature, have been linked to preterm delivery. Levels of total, bound, and free CRH, CRH-binding protein (CRH-BP), and cortisol were measured prospectively in a large sample of pregnant Danish women who delivered preterm and term infants. Measures of maternal serum hormones were taken at 7--23 and 27--37 weeks gestation and, for those who delivered at term, at 37--43 weeks gestation. At 7--23 weeks gestation, maternal levels of total CRH (P = 0.01), bound CRH (P = 0.03), and CRH-BP (P = 0.01) were higher in the preterm than in the term group. At 27--37 weeks gestation, levels of total CRH (P < 0.0001), bound CRH (P < 0.0001), free CRH (P < 0.0001), and cortisol (P < 0.0001) were all higher in the preterm than the term group, whereas levels of CRH-BP (P < 0.0001) were lower in the preterm than in the term group. The best medical and behavioral factors associated with preterm delivery were, respectively, previous preterm delivery (P < 0.0001) and engagement in certain risk-taking behaviors (P = 0.008). The positive relations between preterm delivery and various adverse medical and socioeconomic variables with increases in placental secretion of CRH suggest that the latter may participate in the pathophysiology of preterm delivery.

Preterm birth: associated neuroendocrine, medical, and behavioral risk factors.

Antenatal glucocorticoid administration increases corticotrophin-releasing hormone in maternal plasma

Objective This study was designed to determine whether maternal corticotrophin-releasing hormone (CRH) concentrations are altered after maternal betamethasone administration for fetal lung maturity in women with threatened pretenn labour and whether these effects are dependent on gestational age.



Methods Our study included 49 women with threatened preterm labour who received prenatal betamethasone for fetal lung maturity between 24 and 31 weeks of gestational age and 11 women who did not. Maternal blood was taken before and after glucocorticoid administration or at 24 hours after initial sampling. Plasma CRH, adrenocorticotrophin (ACTH) and cortisol concentrations were determined by radioimmunoassays. The women were stratified into 24–25 weeks, 26–27 weeks, 28–29 weeks, and 30–31 weeks completed gestation.



Results At each gestational age, maternal cortisol concentrations decreased by approximately 85% after glucocorticoid administration. Overall mean cortisol values fell from 580.0 (SD, 351.8) to 89.7 (96.6) nmol/L (n= 40, P < 0.001). Overall mean ACTH values decreased from 9.9 (4.7) to 5.0 (3.4) pmol/L (n= 43, P < 0*001), and the approximate 50% decrease was similar at each gestational age. In marked contrast, overall mean CRH values increased from 58.0 (37.0) to 87.8 (68.6) pmol/L (n= 49, P < 0.001) after betamethasone administration. There was no change in maternal cortisol, ACTH or CRH values over 24 hours in women who did not receive betamethasone.



Conclusions We conclude that maternal betamethasone administration increases maternal plasma CRH values between 24 and 31 completed weeks of gestation.

Antenatal Glucocorticoid Administration Increases Corticotrophin-Releasing Hormone in Maternal Plasma

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Antenatal glucocorticoid administration increases corticotrophin-releasing hormone in maternal plasma

Antenatal Glucocorticoid Administration Increases Corticotrophin-Releasing Hormone in Maternal Plasma