Vitamin D intoxication causes hypercalcaemia by increased bone resorption which responds to pamidronate.

OBJECTIVE

Vitamin D intoxication is a relatively rare but treatable cause of hypercalcaemia. In the past this has been undertaken using corticosteroids. Previous observations have suggested that there is increased bone resorption in hypervitaminosis D. If this were to be the case, specific inhibitors of bone resorption might provide more effective treatment. We have therefore studied the mechanisms of hypercalcaemia and response to therapy in a group of patients with vitamin D intoxication.

DESIGN

Vitamin D metabolites were measured in six patients with vitamin D intoxication; in five of these the components of hypercalcaemia were calculated. These measurements were repeated following treatment with corticosteroids (two patients) or the bisphosphonate, pamidronate (three patients).

RESULTS

In each case the serum 25-hydroxyvitamin D was grossly elevated and there was a more modest elevation in serum 1,25-dihydroxyvitamin D. The components of hypercalcaemia suggest that there was a significant degree of bone resorption in all six patients and that this is the major determinant of hypercalcaemia. Pamidronate treatment resulted in a brisk reduction in plasma calcium concentration. Following corticosteroids the return of calcium to normal was more delayed.

CONCLUSION

The hypercalcaemia of vitamin D intoxication is mediated by increased bone resorption and bisphosphonates have a role in its management.