REMISSION OF HYPOPARATHYROIDISM DURING LACTATION - EVIDENCE FOR A PHYSIOLOGICAL-ROLE FOR PROLACTIN IN THE REGULATION OF VITAMIN-D METABOLISM
REMISSION OF HYPOPARATHYROIDISM DURING LACTATION - EVIDENCE FOR A PHYSIOLOGICAL-ROLE FOR PROLACTIN IN THE REGULATION OF VITAMIN-D METABOLISM
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DOI：
10.1111/j.1365-2265.1987.tb00824.x
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发表时间：
1987-06-01
影响因子：
3.2
通讯作者：
KANIS, JA
中科院分区：
文献类型：
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作者：
CUNDY, T;HAINING, SA;KANIS, JA
我们研究了一名年轻女性与手术甲状旁腺功能减退症，她通常的维持剂量骨化三醇，开发高钙血症产后9天时，哺乳期成立。血清1，25-二羟维生素D3（1，25（OH）2D 3）值非常高（127 pg/ml）。患者未接受外源性骨化三醇治疗40 d，在此期间血清1，25（OH）2D 3水平保持在正常范围内，血清钙下降，半衰期为27 d。当哺乳停止时，骨化三醇的需求量增加到产前水平。骨化三醇的需求量与血清PRL值呈密切的负相关。断奶后，通过增加骨化三醇剂量诱导高钙血症发作。停止骨化三醇后，血清1，25（OH）2D 3在2天内降至低值（4 pg/ml），血清钙在3天的半衰期内下降，需要早期重新引入骨化三醇。我们的结论是，在hypopathyrophic外源性维生素D的需求下降在哺乳期，因为增强内源性生产的1，25（OH）2D 3。因此，与泌乳相关的循环1，25（OH）2D 3浓度的增加是由甲状旁腺非依赖性机制引起的，可能是通过对PRL在1 α-羟色胺上的作用。羟化酶
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 on PRL on the 1.alpha.-hydroxylase.