Abstract
An increasing body of experimental data suggests a role for 24,25(OH)2D3 in bone metabolism. The present study was carried out to assess a possible therapeutic role of this vitamin D metabolite in renal osteodystrophy. Twenty-two chronic dialysis patients, most of whom were previously maintained on 1α(OH)D3 therapy, received additional treatment with 10 μg/day 24,25(OH)2D3 and were compared to 19 patients receiving 1α(OH)D3 alone. Analysis of transiliac bone biopsies obtained at study entry and following 10-16 months of treatment revealed that the combined therapy produced a decrease in bone turnover. Specifically, the addition of 24,25(OH)2D3 inhibited an increase in trabecular bone volume ( BV TV) and suppressed osteoclastic parameters. Thus BV TV increased from 26.2 ± 8.6 to 32.1 ± 7.5% (p < 0.01) in the 1α(OH)D3 group, but it remained unchanged in the combined therapy group. In contrast, the eroded surface ( ES BS), the osteoclast surface ( Oc.S BS), and the osteoclast numbers were significantly suppressed in patients receiving both 24,25(OH)2D3 and 1α(OH)D3, as compared with those receiving 1α(OH)D3 alone (p < 0.01, p < 0.01, and p < 0.001, respectively). These improvements were independent of changes in 1α(OH)D3 dosage. The extent of bone aluminium deposits was unrelated to the administration of 24,25-(OH)2D3 or to its effect. 24,25(OH)2D3 therapy was not associated with any adverse effects.
| Original language | English |
|---|---|
| Pages (from-to) | 369-377 |
| Number of pages | 9 |
| Journal | Bone |
| Volume | 13 |
| Issue number | 5 |
| DOIs | |
| State | Published - 1992 |
Keywords
- 1α(OH)D
- 24,25-(OH)D
- Aluminium
- Bone biopsy
- Dialysis
- Renal osteodystrophy
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