LBODP020 Treatment Of Hypercalcemia Due To Prolonged, Excessive Vitamin D Intake

Abstract

Abstract Case A 66-year-old man with history of anxiety, depression, and complex regional pain syndrome presented to a psychiatric hospital with suicidal ideation. Admission laboratory studies demonstrated hypercalcemia (Ca 14.2 mg/dL) with kidney injury (Cr 3.26). He endorsed taking 5 to 16 (average 8-9) tablets of 1000 IU Vitamin D daily for 10 years. He had heard about the health benefits of Vitamin D and believed it gave him a euphoric effect. Work-up demonstrated elevated ionized calcium (1.63 mmol/L), normal serum phosphorus (3.8 mg/dL), low total protein (6.24 g/dL), normal total albumin (3.42 g/dL), and negative serum protein electrophoresis. Intravenous hydration with normal saline at 200 cc/hr was initiated along with intravenous furosemide. Additional work up demonstrated a suppressed parathyroid hormone level (10pg/ml). 25-hydroxyvitamin D3 (25-(OH)D3) levels were elevated beyond the measurable range (> 155.9 pg/mL). The plasma 1α,25-dihydroxyvitamin D3 (1α,25 (OH)2D3) was normal at 44 pg/mL (range 18-64 pg/mL). With intravenous fluid administration, the patient's ionized calcium level decreased and his creatinine improved. However, 48 hours after the fluids were discontinued on hospital day 3, the ionized calcium and serum creatinine rose once again. Due to the long half-life of Vitamin D and the up-trending calcium levels, he received 60mg of intravenous Pamidronate on hospital day 8. On discharge on hospital day 11, his renal function was stable (Cr 2.24) with normal ionized calcium (1.27 mmol/L). His psychiatric symptoms had resolved. Discussion The two most common causes of hypercalcemia are primary hyperparathyroidism and malignancy. Less commonly, vitamin D-mediated hypercalcemia may result from ectopic 1,25-dihydroxyvitamin D production or excessive Vitamin D ingestion. The known upper limit of daily Vitamin D intake in an adult that will cause no adverse risk is 4000 IU per day. Vitamin D is a fat-soluble vitamin with a half-life of approximately 2 months. The liver converts Vitamin D3 to the metabolite 25-(OH)D3, which has a half-life of 15 days, and the kidney further metabolizes this to 1α,25 (OH)2D3, which has a half-life of 15 hours. Therefore, this patient's 25-(OH)D3 was expected to remain at toxic levels for an unknown time period, placing him at risk of prolonged hypercalcemia with further deterioration of his renal function. There is no standard of care established for patients with vitamin D toxicity. Pamidronate, normally contraindicated for GFR <30 mL/min, was administered after nephrology consultation. Information about vitamin D toxicity is primarily gleaned from case reports and series. This case report serves as a model for study of Vitamin D toxicity in humans for understanding the long-term management in patients with chronic vitamin D toxicosis presenting with renal failure. Presentation: No date and time listed