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The osteodystrophy of hypervitaminosis D: a metabolic study
The Quarterly Journal of Medicine
|October 1, 1986
Summary
Long-term vitamin D2 supplementation led to hypercalcaemia and defective bone mineralization, despite normal vitamin D levels. Cortisone treatment improved calcium balance by reducing active vitamin D metabolites.
Area of Science:
- Endocrinology
- Metabolic Bone Disease
Background:
- Vitamin D is crucial for calcium homeostasis and bone health.
- Excessive vitamin D intake can lead to toxicity, but its effects on bone mineralization are complex.
Observation:
- A patient on daily vitamin D2 for 10 years developed skeletal pain and hypercalcaemia.
- Radiographs revealed osteosclerosis with extensive calcification, while bone histomorphometry showed impaired mineralization.
Findings:
- Despite hypercalcaemia and elevated vitamin D metabolites, the patient exhibited defective bone mineralization and a negative calcium balance.
- Enhanced intestinal calcium absorption and increased urinary hydroxyproline excretion were noted.
Implications:
- This case highlights a rare form of vitamin D toxicity causing impaired bone mineralization.
- Cortisone therapy demonstrated efficacy in managing hypercalcaemia and improving calcium balance by modulating vitamin D metabolism.