REMISSION OF HYPOPARATHYROIDISM DURING LACTATION: EVIDENCE FOR A PHYSIOLOGICAL ROLE FOR PROLACTIN IN THE REGULATION OF VITAMIN D METABOLISM

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Abstract
We studied a young woman with surgical hypoparathyroidism who, on her usual maintenance dose of calcitriol, developed hypercalcaemia 9 d postpartum when lactation was established. Serum values of 1,25‐dihydroxyvitamin D3 (1,25(OH)2D3) values were very high (127 pg/ml). The patient remained without exogenous calcitriol treatment for 40 d, during which time serum 1,25(OH)2D3 levels remained within the normal range and serum calcium fell with a half‐time of 27 d. The requirements for calcitriol increased to antepartum levels when lactation had ceased. There was a close negative correlation between requirements for calcitriol and serum PRL values. After weaning, an episode of hypercalcaemia was induced by increasing the dose of calcitriol. On stopping calcitriol the serum 1,25(OH)2D3 fell to low values (4 pg/ml) within 2 d and serum calcium fell with a half‐time of 3 d, necessitating the early reintroduction of calcitriol. We conclude that in hypoparathyroidism exogenous vitamin D requirements fall during lactation because of enhanced endogenous production of 1,25(OH)2D3. The lactation‐associated increase in circulating 1,25(OH)2D3 concentrations thus results from a parathyroid hormone‐independent mechanism, possibly by an effect of PRL on the la‐hydroxylase.
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