Persistent Symptomatic Hypercalcemia Associated with Long-Term Unmonitored Ergocalciferol Exposure

Presentation Number: MON 327
Date of Presentation: April 3rd, 2017

Amanda Kile* and Natallia Maroz
Kettering Medical Center, Kettering, OH


Background: Persistent symptomatic hypercalcemia from vitamin D toxicity is rare. Ergocalciferol is a prescribed Vitamin D2 analogue, which should require monitoring in all patients. This fat soluble pro-vitamin has a half-life of 2-3 weeks. Here we present a case of prolonged ergocalciferol exposure resulting in symptomatic hypercalcemia.

Case: 82yo female with PMH of HTN, HLD, hypothyroidism and CKD stage 4 (baseline creatinine 1.5-2.0 mg/dL) was admitted with confusion, hallucinations and diarrhea. Family reported weight loss and anorexia. She had history of thyroidectomy with parathyroidectomy at age 23 and subsequently took daily calcium and weekly ergocalciferol 50,000 IU supplementation for an unknown number of years without monitoring.

On presentation, vitals were normal, BMI 18.8 kg/m2, and the patient appeared confused with poor skin turgor and dry mucous membranes. Renal panel demonstrated elevated BUN 78 mg/dL(3-29), Cr 5.2 mg/dl(0.5-1.2) and calcium level 13.4 mg/dL(8.5-10.5). Intact PTH was mildly suppressed at 12 pg/mL(15-65) and total vitamin D, 25-OH level was notably elevated at 160 ng/mL(20-100). PTH-like peptide, vitamin D 1,25(OH)2, albumin, and ACE levels were within normal range. Urine calcium was found to be upper-normal at 236 mg/day(100-250). Renal ultrasound showed non-obstructing nephrolithiasis and a bladder stone, which required surgical removal. Stone analysis resulted as calcium apatite (a crystal type of calcium phosphate). Upon review and in finding no evidence of monoclonal gammopathy, malignancy or granulomatous disease, it was determined her hypercalcemia was due to ergocalciferol toxicity likely from unmonitored long-term supplementation.

Her elevated vitamin D, 25-OH and calcium levels were resistant to intravenous fluids, loop diuretics, and calcitonin administration. Two doses of IV pamidronate provided only short-term improvement of serum calcium level. Thus, oral prednisone was initiated with clinical improvement, normalization of hypercalcemia, and betterment of her renal function. Over 12-month follow-up with continual prednisone therapy, calcium levels and renal function have stabilized, however vitamin D levels have remained elevated.

Conclusion: This case demonstrates severe persistent hypercalcemia in a setting of unmonitored long-term ergocalciferol intake. Despite conventional treatment, our patient had continued supratherapeutic vitamin D, 25-OH levels beyond one year of abstinence from supplementation. This case demonstrates that although symptomatic vitamin D-induced hypercalcemia is rare, the clinical course can be arduous if treatment is refractory. Such morbidity could be avoided if appropriate frequency of monitoring serum levels is implemented.


Nothing to Disclose: AK, NM