ODP123 Severe Hypercalcemia During Lactation In A Patient With Pre-Existing Hypoparathyroidism

Abstract

Abstract Background Pregnancy and lactation are associated with profound changes in calcium homeostasis that can complicate the management of primary hypoparathyroidism. Clinical Case A 35-year-old woman with a history of post-operative hypoparathyroidism aftertotal thyroidectomy for metastatic papillary thyroid carcinomawas found to have hypercalcemia during lactation, two months after delivery of her first pregnancy. She was taking calcitriol 0.5mcgtwo times daily prepartum, which she continued throughout pregnancy and postpartum. Two weeks prior to delivery, her serum calcium was 9.7 mg/dL (n: 8.6-10.3 mg/dL). However, testingtwo months postpartum revealed a markedly elevated serum calcium 13.7 mg/dL and ionized calcium 1.70 mmol/L (n: 1. 09-1.29 mmol/L). Subsequent workup was notable for low parathyroid hormone (PTH) 4 pg/mL (n: 11-51 pg/mL), and normal PTH-related protein (PTHrP) 0.3 pmol/L (n: <2 pmol/L), 25-hydroxy-vitamin D 60 ng/mL (n: 30-80 ng/mL), and 1,25-dihydroxy-vitamin D 38. 0 pg/mL (n: 19.9-79.3 pg/mL). Her calcitriol was reducedto 0.25mcg once daily, and her serum and ionized calcium improved to 10.2 mg/dL and 1.18 mmol/L, respectively, within 10 days. Two years later, after her second pregnancy, she again developed hypercalcemia during lactation. One month prior to delivery, her serum calcium was 8. 0 mg/dL and her ionized calcium was 1. 04 mmol/L on a regimen of calcium carbonate 1000mg three times daily and calcitriol 0.5mcg twice daily. However, two months after delivery and during lactation, her serum and ionized calcium increased to 10.4 mg/dL and 1.31 mmol/L, respectively. Evaluation of her PTHrP levels revealed an increase from 13 pg/mL (n: 14-27 pg/mL) one-year prepartum to 22 pg/mL during her third trimester, and then to17 pg/mL two months postpartum. In addition, her 1,25-dihydroxy-vitamin D increased from 60.2 pg/mL one-year prepartum to 108. 0 pg/mL during her third trimester and decreased to 70.2 pg/mL two months postpartum. Reductions in her calcium and calcitriol regimen improved her serum and ionized calcium levels. Conclusion This rare case highlights the changes in calcium physiology during pregnancy and lactation that can significantly alter calcium and calcitriol requirements in women with primary hypoparathyroidism. During pregnancy, calcium demand is met by increased placental and fetal PTHrP secretion and increased 1,25-dihydroxy-vitamin D production from placental 1-alpha-hydroxylase activity. Conversely, during lactation, this demand is met by increased net bone resorption from PTHrP produced by the mother's mammary tissue and decreased estrogen levels postpartum. As illustrated in this case, continuation of prepartum calcium and calcitriol regimens during pregnancy and lactation can result in maternal hypercalcemia. Thus, close monitoring of calcium levels during pregnancy and lactation in women with hypoparathyroidism is essential to adjust calcium and calcitriol supplementation and maintain adequate calcium homeostasis in the mother and fetus. Presentation: No date and time listed