MON-379 A Case of Eucalcemic Parathyroid Hormone Elevation with Hypercalciuria

Abstract T. Othman: None. J.Q. Dai-Ju: None. Background: Normocalcemic hyperparathyroidism is a condition frequently referred to endocrine for evaluation. It can be caused by normocalcemic primary hyperparathyroidism (NPHPT) or secondary hyperparathyroidism (SHPT). Differentiating between the two conditions can be very challenging. There are a variety of medical conditions and medications that can induce secondary hyperparathyroidism, including chronic kidney disease, malabsorption, idiopathic hypercalciuria, vitamin D deficiency, calcium deficiency, and Paget’s disease of bone (1). Clinical Case: 61-year-old female with past medical history of obesity s/p sleeve gastrectomy five years prior, Roux-en-Y gastric bypass (RYBG) two years prior, hypertension, vitamin D deficiency, hypercalciuria, and nephrolithiasis who was initially referred to surgery for evaluation of parathyroidectomy. Serum calcium levels ranged 8.3 to 9.1 mg/dL (normal 8.6-10.3), with intact PTH levels 88-211 pg/mL (normal 16-77). The ionized calcium was 4.9 mg/dL (normal 4.7-5.5), 25OHD 31mg/dL, and urinary calcium 416 mg/24H. DEXA revealed T-scores of -1.5 to 0.2. Parathyroid scan, ultrasound exam and four-dimensional parathyroid CT failed to localize parathyroid adenoma. Patient was referred to endocrinology for further evaluation. Patient was presumed to have SHPT due to bariatric surgery, and was treated with calcium citrate about 500 mg elemental three times daily and vitamin D3 5000 IU daily. After four months, repeated serum calcium level was stable at 8.8 mg/dL, with intact PTH 139 pg/ml, 25OHD 36 mg/dL, and elevated urinary calcium 303 mg/24H. The patient was started on hydrochlorothiazide 12.5 mg daily, which was later changed to chlorthalidone 25 mg daily. Urinary calcium normalized to 141 mg/24H. In the following two years, calcium was consistently normal 8.8-9.1 mg/dL, and intact PTH gradually decreased to 107, 84, and finally normalized 64 pg/mL. The ionized calcium was unchanged 4.9 mg/dL, 25OHD 39 mg/dL. In this case of SHPT after RYBG with coexisting idiopathic hypercalciuria, calcium citrate and vitamin D plus thiazide therapy was the proper treatment. Conclusion: Most cases of elevated PTH levels with normal ionized calcium levels are due to SHPT rather than NPHPT. Correct diagnosis is very important for subsequent management (2). Medical conditions and medications that may cause SHPT should first be evaluated and corrected in order to avoid unnecessary imaging tests and surgeries following a misdiagnosis of NPHPT. Reference: Shaker JL & Wermers R. The Eucalcemic Patient with Elevated Parathyroid Hormone Levels. Journal of the Endocrine Society. 2023. 7:1-12. Bilezikian JP, Khan AA, Silverberg SJ, et al. Evaluation and man- agement of primary hyperparathyroidism: summary statement and guidelines from the fifth international workshop. J Bone Mineral Res. 2022. 37(11):2293-2314. Monday, June 3, 2024