Division of Endocrinology and Metabolism, Calcium Disorders Clinic, Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
Mayo Clinic, Endocrinology Transplant Center, Rochester, Minnesota, USA.
Eur J Endocrinol. 2019 Feb 1;180(2):R37-R44. doi: 10.1530/EJE-18-0541.
Purpose Review calcium homeostasis in pregnancy and provide evidence-based best practice recommendations for the management of hypoparathyroidism in pregnancy. Methods We searched MEDLINE, EMBASE and Cochrane databases from January 2000 to April 1, 2018. A total of 65 articles were included in the final review. Conclusions During pregnancy, calcitriol levels increase by two- to-three-fold resulting in enhanced intestinal calcium absorption. The renal filtered calcium load increases leading to hypercalciuria. PTHrP production by the placenta and breasts increases by three-fold, and this may lower the doses of calcium and calcitriol required during pregnancy in mothers with hypoparathyroidism. The literature however describes a wide variation in the required doses of calcium and calcitriol during pregnancy in hypoparathyroid mothers, with some women requiring higher doses of calcitriol, whereas others require lower doses. Close monitoring is necessary as hypercalcemia in the mother may suppress the fetal parathyroid gland development. Also hypocalcemia in the mother is harmful as it may result in secondary hyperparathyroidism in the fetus. This may be associated with demineralization of the fetal skeleton and the development of intrauterine fractures. Inadequate treatment of hypoparathyroidism may also result in uterine contractions and an increased risk of miscarriage. Treatment targets during pregnancy are to maintain a low normal serum calcium. Calcium, calcitriol and vitamin D supplements are safe during pregnancy. Close monitoring of the mother with a multidisciplinary team is advised for optimal care. If calcium homeostasis is well controlled during pregnancy, most women with hypoparathyroidism have an uncomplicated pregnancy and give birth to healthy babies.
回顾妊娠期间钙稳态,并为妊娠期间甲状旁腺功能减退症的管理提供循证最佳实践建议。
我们检索了 2000 年 1 月至 2018 年 4 月 1 日的 MEDLINE、EMBASE 和 Cochrane 数据库。共有 65 篇文章纳入最终综述。
妊娠期间,1,25-二羟维生素 D3 水平增加 2-3 倍,导致肠道钙吸收增强。肾脏滤过的钙负荷增加导致尿钙增加。胎盘和乳房产生的甲状旁腺激素相关蛋白增加 3 倍,这可能降低甲状旁腺功能减退症母亲在妊娠期间对钙和 1,25-二羟维生素 D3 的需求量。然而,文献描述了甲状旁腺功能减退症母亲在妊娠期间对钙和 1,25-二羟维生素 D3 的需求量存在很大差异,有些女性需要更高剂量的 1,25-二羟维生素 D3,而有些女性则需要较低剂量。需要密切监测,因为母亲的高钙血症可能会抑制胎儿甲状旁腺的发育。此外,母亲的低钙血症也是有害的,因为它可能导致胎儿继发性甲状旁腺功能亢进。这可能与胎儿骨骼脱矿和宫内骨折的发展有关。甲状旁腺功能减退症治疗不足也可能导致子宫收缩和流产风险增加。妊娠期间的治疗目标是维持血清钙低正常水平。钙、1,25-二羟维生素 D3 和维生素 D 补充剂在妊娠期间是安全的。建议多学科团队密切监测母亲,以获得最佳护理。如果妊娠期间钙稳态得到很好的控制,大多数甲状旁腺功能减退症妇女的妊娠过程通常较为顺利,并生下健康的婴儿。