SAT191 Primary Hyperparathyroidism With Low-Normal Parathyroid Hormone Levels: Phosphorus Can Be The Key

Abstract

Abstract Disclosure: D. He: None. T. Tavdy: None. Y. Tomer: None. D. Kalbi: None. V. Tabatabaie: None. Background: Primary hyperparathyroidism (PHPT) is characterized by the inappropriate secretion of PTH that leads to hypercalcemia. In patients with PHPT, 80-90% have PTH levels above the normal range and 10-20% have inappropriately “normal” PTH levels, most often in the high-normal range1. PTH levels below or in the lower end of the normal range prompt investigation of non-PTH mediated causes of hypercalcemia. We present a case of PHPT with low-normal PTH levels, and discuss how phosphorus levels guided our diagnosis of an underlying parathyroid adenoma. Clinical Case: An 83-year-old woman was found to have hypercalcemia with corrected calcium ∼13 mg/dL (8.5 - 10.5 mg/dL) and PTH of 36.7 pg/mL (20.0 - 80.0 pg/mL). Phosphorus was consistently low, ranging from 2.1 to 2.4 mg/dL (2.5 - 4.5 mg/dL). PTHrP was 18 pg/mL (11-20 pg/mL). 25-hydroxy vitamin D was 24.5 ng/mL (30-60 ng/mL). 1,25-dihydroxy vitamin D was 36 pg/mL (18-72 pg/mL). Serum and urine protein electrophoresis were normal. HTLV-1/2 antibody was negative. TSH was 1.15 uU/mL (0.30 - 4.20 uU/mL). The patient had no history of ingesting lithium or thiazide diuretics. Suspecting PHPT, the patient underwent a nuclear medicine parathyroid scan which showed abnormal parathyroid tissue in the left thyroid lobe. In the setting of volume overload, management of the patient’s persistent hypercalcemia of greater than 12 mg/dL (8.5 - 10.5 mg/dL) began initially with a dose of pamidronate 60 mg and gentle hydration followed by furosemide. Corrected calcium improved to 12.3 mg/dL (8.5 - 10.5 mg/dL). Given the patient’s decreased functional status (bedbound) and high surgical risk, after discussion with the patient and her family, a decision was made to proceed with medical management and not with parathyroidectomy. She was treated with cinacalcet 30 mg twice daily. The goal calcium of < 1 unit over the upper limit of normal (11.5 mg/dL) was achieved on day of discharge of the patient back to her nursing home. Conclusion: In patients with hypercalcemia, low serum phosphorus can point to a PTH- or PTHrP-mediated process. Inappropriate secretion of PTH or PTHrP results in high serum calcium and low phosphorus levels by increasing bone resorption and renal calcium reabsorption, and decreasing renal phosphorus reabsorption. This case shows that in patients with hypercalcemia and concomitant hypophosphatemia with normal PTHrP, PHPT should still be considered as a potential etiology, even in the setting of a low-normal PTH level. In our patient, the presence of a parathyroid adenoma was demonstrated with a conclusive parathyroid scan.