Objective: Hypercalcemia in a patient with Graves disease can occur in up to 22% of cases. The mechanism is thought to be increased bone resorption. There are more rare causes of hypercalcemia in these patients with hyperthyroidism, such as hyperparathyroidism, which occurs in less than 1% of patients. We describe a rare occurrence of primary hyperparathyroidism due to multiple endocrine neoplasia type 1 (MEN 1) in a Graves disease patient presenting with hyperthyroidism and hypercalcemia.Methods: The patient initially presented with a 3-week history of nausea, vomiting, and abdominal pain. She also had an 8-week history of a 12-pound weight loss. She was diagnosed with hyperthyroidism secondary to Graves disease and was noted to have concurrent hypercalcemia. She was diagnosed with primary hyperparathyroidism. The patient underwent subtotal thyroidectomy and total parathyroidectomy with forearm autotransplantation. Subsequent genetic testing confirmed the diagnosis of MEN 1.Results: A review of the literature was conducted to identify previous studies pertaining to concurrent hypercalcemia in hyperthyroid patients, focusing on reports related to their diagnosis and management.Conclusion: Co-existing primary hyperparathyroidism due to MEN 1, although rare, should be considered in a patient with hyperthyroidism and hypercalcemia. A thorough evaluation is necessary to avoid a delay in the correct diagnosis and treatment of the underlying conditions. Clinicians should be aware of the rare occurrence of primary hyperparathyroidism due to MEN 1 in a Graves disease patient presenting with hyperthyroidism and hypercalcemia. (AACE Clinical Case Rep. 2019;5:e13-e15) Abbreviations: MEN 1 = multiple endocrine neoplasia type 1; PTH = parathyroid hormone

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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

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