INTRODUCTIONGlucocorticoids are vital for normal foetal growth and organ development, but foetal overexposure to the major circulating glucocorticoid, cortisol, is associated with intrauterine growth restriction and an increased risk of cardiovascular disease in later life. During pregnancy, a number of endocrine changes cause the maternal hypothalamic‐pituitary‐adrenal (HPA) axis to undergo dramatic activation resulting in cortisol levels that are around threefold higher than in nonpregnancy. Dysregulation of the maternal HPA axis has been implicated in pregnancy complications including preterm birth and preeclampsia. The glucocorticoid corticosterone, which is known to circulate at significantly lower levels than cortisol in nonpregnancy, is increasingly being recognized as a key player in HPA axis regulation. It has been suggested that the foetus preferentially secretes corticosterone over cortisol in response to stress, and therefore has been proposed to be an important biomarker of foetal stress at the time of delivery, but little is known about how it changes during pregnancy.The circadian rhythm of the HPA axis, which in humans is characterized by peak levels of cortisol early in the morning, is maintained in pregnancy. More detailed studies of circadian rhythmicity in animals and in nonpregnant humans have identified an underlying “ultradian rhythm” of cortisol pulses within
Clinical Endocrinology – Wiley
Published: Jan 1, 2018
Keywords: ; ; ;
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