Endocrine Abstracts

Maternal calcium homeostasis undergoes major adaptations during pregnancy and lactation to meet the requirements of the developing fetus and infant. Early pregnancy is characterised by accrual of calcium in the maternal skeleton, which begins in the first trimester. This is mediated by a 2-5-fold increase in the synthesis of calcitriol by the renal proximal tubule, which leads to a doubling of intestinal calcium absorption during pregnancy. The increased calcitriol synthesis occurs independently of parathyroid hormone (PTH), and may instead be mediated by pregnancy hormones such as oestradiol, prolactin or human placental lactogen. Maternal circulating parathyroid hormone-related peptide (PTHrP) increases progressively throughout pregnancy and may also promote renal calcitriol synthesis. Increased intestinal calcium absorption suppresses PTH secretion and increases urine calcium excretion during pregnancy. Fetal accrual of calcium for skeletal development occurs mainly during the third trimester is supported by maternal increases in both calcium absorption and bone resorption. After childbirth, maternal calcium homeostasis involves a shift from renal calcitriol synthesis to increased mammary synthesis of PTHrP. High levels of PTHrP combined with lactational amenorrhoea and a hypo-oestrogenic state promote bone resorption in order to provide calcium for milk production. Thus, pregnancy and lactation are characterised by unique PTH-independent mechanisms for supplying calcium for fetal and infant development.