Maternal hypothalamic-pituitary-adrenal axis in pregnancy and the postpartum period. Postpartum-related disorders.

Abstract

During pregnancy, placenta-derived CRH increases exponentially in the plasma. Circulating levels of CRH-binding protein decrease considerably in the last trimester of pregnancy, resulting in further elevation of bioavailable plasma CRH. The adrenal glands during pregnancy gradually become hypertrophic because of the increase in ACTH, which parallels that of CRH. Thus, pregnancy is a transient period of relative hypercortisolism. The activation of the hypothalamic-pituitary-adrenal axis during pregnancy has been proposed to function as a biological clock. In this model, the placenta is perceived as a stress-sensitive organ and placental CRH as a timing starter, determining a preterm, term, or postterm labor. During pregnancy, as well as during the immediate postpartum period, the hypothalamic maternal CRH secretion is suppressed, because of the circulating levels of cortisol. Hypothalamic CRH secretion normalizes within 12 weeks. This transient postpartum maternal hypothalamic CRH suppression, together with the steroid withdrawal that follows parturition, might be causally related to the mood disorders and the vulnerability to autoimmune diseases such as thyroiditis or rheumatoid arthritis often observed during the postpartum period.