Pituitary disorders in pregnancy

Abstract

The management of pituitary disorders in pregnancy presents a unique challenge for maternal medicine specialists and endocrinologists. Advances in assisted reproductive technologies (ART) mean that women with hypopituitarism are increasingly able to conceive. The pituitary undergoes significant physiological changes during pregnancy. Pituitary hormone replacement regimens must therefore be adjusted throughout pregnancy in an attempt to mimic these changes. Close clinical and biochemical follow-up and collaboration across specialties is essential to ensure optimal maternal and fetal outcomes. Although many women with hypopituitarism will have a normal pregnancy, rates of miscarriage, labour induction and caesarean sections are higher than the general population. Most women with hypopituitarism are diagnosed prior to pregnancy; however, some pituitary disorders including lymphocytic hypophysitis, Sheehan's syndrome and pituitary apoplexy have a predilection to arise during pregnancy or the postpartum period. Prompt recognition of these disorders is essential to prevent potentially fatal complications and optimise maternal and fetal wellbeing.

Keywords: Fertility; Hypopituitarism; Maternal health; Pituitary disorders; Pregnancy.

Graphical abstract

Fig. 1

Influence of the placenta on pituitary physiology. Corticotropin-releasing hormone (CRH) release from the placenta stimulates ACTH and cortisol secretion. Oestradiol induces the synthesis of cortisol-binding globulin. These adaptations increase both elevated free and bound cortisol levels. High oestradiol concentrations supress pituitary gonadotropins throughout pregnancy. Human chorionic gonadotropin (hCG) stimulates free T4 (fT4) production, with compensatory declines in TSH in the first trimester. Oestradiol also induces relative growth hormone resistance, resulting in insulin-like growth factor-1 (IGF-1) declining by approximately 30% in the first trimester. The placenta produces GH-V, a growth hormone isoform, from 8 weeks gestation. GH-V can overcome GH resistance, resulting in increased IGF-1 levels and a compensatory decline in pituitary GH by mid-pregnancy. AVP controls salt and water homeostasis by stimulating water reabsorption from the kidneys. Metabolism of AVP increases three- to fourfold due to placental vasopressinase. This may unmask pre-existing partial AVP deficiency (formerly called cranial diabetes insipidus) in the second and third trimesters. Oxytocin is responsible for initiating labour and stimulating uterine contractility. It is also thought to play a role in modulating behaviour and mother–baby bonding.

Fig. 2

Management of hypopituitarism in pregnancy.