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Management of hypercalcaemia due to hypervitaminosis D

Vitamin D deficiency is a common diagnosis and consumer use of over-the-counter vitamin D supplementation is potentially unregulated, unreported and unmonitored. Here, we report a case of an elderly woman who presented with symptomatic severe hypercalcaemia due to hypervitaminosis D due to excessive oral vitamin D3 (cholecalciferol) supplementation. An 82-year-old woman with a history of hypothyroidism, hypertension, chronic obstructive pulmonary disease, vertigo and chronic fatigue syndrome was admitted to hospital with an 8-week history of lethargy. Examination revealed a blood pressure of 193/77 mmHg and she was clinically dehydrated. Initial investigations demonstrated significantly elevated corrected calcium of 3.95 (2.15–2.65 mmol/L) and ionised calcium 2.11 (1.15–1.30 mmol/ L). Serum phosphate was normal at 1.42 (0.75–1.50 mmol/L) and parathyroid hormone (PTH) was low but not fully suppressed at 1.0 (2.0–8.5 pmol/L). She had evidence of acute kidney injury with creatinine 110 (40–90 μmol/L) and estimated glomerular filtration rate (eGFR) 40 (baseline 85 mL/min/1.73 m). Initial vitamin D level was >375 nmol/L, which on 1:2 manual dilution approximated to 700 nmol/L. The patient admitted to taking 90 000 IU cholecalciferol, which she purchased online, daily for the preceding 2 months. Initial treatment included aggressive intravenous fluid administration and calcitonin followed by oral prednisolone 25 mg daily, with significant reduction in serum calcium to 3.49 mmol/L on Day 5 and 3.02 mmol/L on Day 8 of admission. On Day 10, mild hypercalcaemia (2.90 mmol/L) persisted and subcutaneous denosumab 60 mg was administered. The serum calcium returned within normal range by Day 15 and stabilised at 2.30 mmol/L 3 weeks postdischarge (Fig. 1). Serum vitamin D declined to 338 nmol/L by this time. Renal dysfunction persisted with eGFR 55 mL/min/1.73 m, despite correction of hypercalcaemia, and extensive investigations including serum protein electrophoresis were unremarkable. Vitamin D plays a vital role in bone metabolism, calcium and phosphate homeostasis, PTH production and immunity. There have been reports of hypercalcaemia due to high-dose vitamin D supplementation with daily doses of 4000 IU/d (or higher) or single doses of 300 000 IU; however, this is uncommon and resulting hypercalcaemia mild and transient. Ingestion of large amounts of cholecalciferol leads to storage in adipose tissue, which may be released slowly over time. As lipid stores become saturated, serum levels rise. Hypercalcaemia with calcium >3.0 mmol/L accompanied with changes in sensorium requires inpatient management. This usually comprises volume expansion with isotonic saline, salmon calcitonin and intravenous bisphosphonates. Salmon calcitonin therapy is limited to 72 h due to development of tachyphylaxis. Bisphosphonates may be contraindicated in renal impairment, as in the present case. Denosumab has proven efficacy in treatment of malignant hypercalcaemia, but there is limited evidence for its use in hypercalcaemia in other settings. It inhibits bone resorption, one of the mechanisms through which hypervitaminosis D leads to hypercalcaemia.