Hypercalcemia and hyperosteolysis in vitamin D intoxication: effects of clodronate therapy

Bone. 1994 Mar-Apr;15(2):193-8. doi: 10.1016/8756-3282(94)90707-2.

Abstract

Vitamin D intoxication is a rare cause of hypercalcemia, which is associated with severe and prolonged morbidity. Hypercalcemia and/or hypercalciuria are the consequence of increases in both intestinal absorption and bone resorption. We report on 7 cases of vitamin D overdose (25-hydroxyvitamin D: 710 +/- 179 nmol/l; normal range: 20-90). The indications for vitamin therapy were osteoporosis (5), hypoparathyroidism (1), and osteomalacia (1). Enhanced bone resorption was demonstrated by increased fasting urinary calcium excretion (0.192 +/- 0.067 mmol/l GFR, normal < 0.045). Sequential biochemical measurements in the hypoparathyroid patient showed the persistence of abnormally elevated fasting urinary calcium and of serum 25-hydroxyvitamin D concentrations, even after normalization of plasma calcium, emphasizing that enhanced bone resorption is a prominent feature of vitamin D action. The intravenous administration of a single infusion of the bisphosphonate clodronate to 3 patients led to a correction of hypercalcemia/hypercalciuria, whereas prednisone therapy given to 2 other cases barely affected the abnormal biochemical values. These results indicate that enhanced bone resorption encountered in vitamin D intoxication could be favorably influenced by bisphosphonate treatment.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Calcium / urine
  • Clodronic Acid / therapeutic use*
  • Drug Overdose / complications
  • Female
  • Humans
  • Hypercalcemia / chemically induced
  • Hypercalcemia / drug therapy*
  • Hypercalcemia / physiopathology
  • Male
  • Middle Aged
  • Osteolysis / chemically induced
  • Osteolysis / drug therapy*
  • Osteolysis / physiopathology
  • Vitamin D / poisoning*

Substances

  • Clodronic Acid
  • Vitamin D
  • Calcium