Severe Hypercalcemia During Lactation in a Patient With Pre-existing Hypoparathyroidism
Source: PubMed Central Open Access, NCBI / U.S. National Library of Medicine
Calcium homeostasis undergoes significant physiologic changes during pregnancy and lactation to support fetal skeletal development and neonatal calcium needs. During pregnancy, calcium requirements are met by increased activation of 1,25-dihydroxyvitamin D (1,25-(OH)D) by placental 1a-hydroxylase and by increased maternal and placental secretion of parathyroid hormone-related protein (PTHrP). Conversely, during lactation, calcium demand is met by maternal bone resorption driven by postpartum decline in estrogen levels and by PTHrP produced by maternal breast tissue. These physiologic adaptations complicate the management of patients with primary hypoparathyroidism, who require calcium and calcitriol supplementation to maintain eucalcemia. Herein, we describe a case of a 35-year-old woman with post-operative hypoparathyroidism following total thyroidectomy for metastatic papillary thyroid carcinoma who developed hypercalcemia during lactation after each of her two pregnancies. Reducing her calcium and calcitriol supplementation rapidly normalized her calcium levels. This case highlights how physiologic changes in calcium metabolism during pregnancy and lactation can significantly alter calcium and calcitriol requirements in patients with hypoparathyroidism. Continuation of prepartum calcium and calcitriol regimens during pregnancy and lactation can cause maternal hypercalcemia. Thus, close surveillance of calcium levels in women with hypoparathyroidism is essential to adjust c
Abstract
Calcium homeostasis undergoes significant physiologic changes during pregnancy and lactation to support fetal skeletal development and neonatal calcium needs. During pregnancy, calcium requirements are met by increased activation of 1,25-dihydroxyvitamin D (1,25-(OH)D) by placental 1a-hydroxylase and by increased maternal and placental secretion of parathyroid hormone-related protein (PTHrP). Conversely, during lactation, calcium demand is met by maternal bone resorption driven by postpartum decline in estrogen levels and by PTHrP produced by maternal breast tissue. These physiologic adaptations complicate the management of patients with primary hypoparathyroidism, who require calcium and calcitriol supplementation to maintain eucalcemia. Herein, we describe a case of a 35-year-old woman with post-operative hypoparathyroidism following total thyroidectomy for metastatic papillary thyroid carcinoma who developed hypercalcemia during lactation after each of her two pregnancies. Reducing her calcium and calcitriol supplementation rapidly normalized her calcium levels. This case highlights how physiologic changes in calcium metabolism during pregnancy and lactation can significantly alter calcium and calcitriol requirements in patients with hypoparathyroidism. Continuation of prepartum calcium and calcitriol regimens during pregnancy and lactation can cause maternal hypercalcemia. Thus, close surveillance of calcium levels in women with hypoparathyroidism is essential to adjust calcium and calcitriol supplementation and avoid hypercalcemia.