Abstract #1399984: Hypercalcemia Secondary to Vitamin D Toxicity Treated with Glucocorticoids

Abstract

Vitamin D toxicity is a rare cause of hypercalcemia and there is no consensus on active treatment. Though glucocorticoids can decrease intestinal calcium absorption, increase urinary calcium excretion, and reduce levels of biologically active vitamin D metabolites, its use in vitamin D toxicity is controversial. Here we present a case of hypercalcemia secondary to hypervitaminosis D treated with glucocorticoids. A 77-year-old female with a history of vitamin D deficiency and prior admission for hypercalcemia attributed to lithium use (discontinued in December 2021) presented to the emergency room for hypercalcemia on outpatient labs. Labs were notable for calcium 14.6 mg/dL, albumin 3.8 g/dL, ionized calcium above detectable limits (>7.3 mg/dL), PTH 22.9 pg/mL, 25-OH vitamin D 135 ng/mL, 1,25-OH vitamin D 67.2 pg/mL (reference range: 19.9-79.3 pg/mL), estimated GFR 23 mL/min/1.73 m2, and undetectable lithium level. Additional workup included normal SPEP/UPEP, parathyroid hormone-related peptide, retinol and retinyl palmitate vitamin A, and computed-tomography of the chest, abdomen, and pelvis without signs of malignancy. History obtained from family revealed the patient had been supplementing with at least 10,400 IU of cholecalciferol daily, along with at least 180 mg of calcium daily (unknown if elemental or calcium carbonate). She was hydrated with isotonic intravenous fluids, given calcitonin 4 units/kg for 3 days, and prednisone 20 mg daily for 2 days. Following day 3 of calcitonin, prednisone was replaced with hydrocortisone 40 mg twice daily. Calcium improved to 10.8 mg/dL and she was discharged on hydrocortisone at same dose and frequency. Upon two-week follow up, calcium had improved to 10.0 mg/dL thus hydrocortisone was tapered to 20 mg twice daily. Due to a misunderstanding, she discontinued hydrocortisone resulting in an increased calcium of 12.2 mg/dL several weeks later. Four weeks upon resumption of hydrocortisone, the calcium improved to 10.2 mg/dL and the hydrocortisone was tapered to 10 mg twice daily. Five weeks later (approximately 4 months since starting hydrocortisone), the calcium was 10.4 mg/dL, the PTH was 19 pg/mL, and 25-OH vitamin D was 37.1 ng/mL. There are no guidelines or consensus on the treatment for vitamin D-induced hypercalcemia. In this case, glucocorticoids were shown to be an effective treatment for hypercalcemia secondary to vitamin D toxicity; the worsening of hypercalcemia upon accidental discontinuation and resolution following resumption of hydrocortisone further supports this conclusion. Though the expected duration of treatment is unclear, our case suggests long-term glucocorticoids are likely necessary.