INFLUENCE OF 1α-(OH)D3 ADMINISTRATION ON BONE AND BONE MINERAL METABOLISM IN PATIENTS ON CHRONIC GLUCOCORTICOID TREATMENT; A DOUBLE BLIND CONTROLLED STUDY
Article first published online: 17 MAR 2008
Volume 19, Issue 2, pages 265–273, August 1983
How to Cite
BRAUN, J. J., BIRKENHÄGER-FRENKEL, D. H., RIETVELD, A. H., JUTTMANN, J. R., VISSER, T. J. and BIRKENHÄGER, J. C. (1983), INFLUENCE OF 1α-(OH)D3 ADMINISTRATION ON BONE AND BONE MINERAL METABOLISM IN PATIENTS ON CHRONIC GLUCOCORTICOID TREATMENT; A DOUBLE BLIND CONTROLLED STUDY. Clinical Endocrinology, 19: 265–273. doi: 10.1111/j.1365-2265.1983.tb02989.x
- Issue published online: 17 MAR 2008
- Article first published online: 17 MAR 2008
- (26 October 1982; 3 February 1983; 16 February 1983
We have performed a double-blind placebo controlled study of 1α-hydroxyvita-min D3 (1α-(OH)D3) 2 μg daily for 6 months, in 14 patients receiving long-term glucocorticoid treatment. Patients were matched for age, sex, underlying disease and dose of glucocorticoid.
Initial values for serum calcium, phosphorus and alkaline phosphatase were in the normal range. Two of the 14 patients showed an increased serum immunoreactive parathyroid hormone (iPTH) concentration. Serum 25-hyd-roxyvitamin D and 1,25-dihydroxyvitamin D (l,25-(OH)2D) were normal but the average 24,25-dihydroxyvitamin D (24,25-(OH)2D) was low.
The histomorphometrically determined trabecular bone volume of an iliac crest biopsy appeared to be low in 6 patients. The average active bone resorption and osteoid seams were increased, while the average osteoblast seams were within the normal range. Treatment with 1α-(OH)D3 raised 47Ca2+ intestinal absorption and 24 h urinary Ca2+ excretion significantly at 3 and 6 months and at 6 months serum iPTH concentration and 24 h urinary hydroxyproline excretion had fallen significantly in the treated group. During treatment with 1α-(OH)D3 the serum 1,25-(OH)2D and 24,25-(OH)2D levels increased significantly.
In all cases of the 1α-(OH)D3-group, the second bone biopsy, taken at the end of the treatment period, showed a decrease of active resorption and a more positive course of trabecular bone volume than the biopsy of the placebo-treated counterpart: trabecular bone volume remained constant or even increased in the 1α-(OH)D3-group. In both groups osteoid seams and osteoblast seams did not change significantly. We conclude that treatment with 1α-(OH)D3 during 6 months inhibits the increased bone resorption seen in glucocorticoid-induced bone disease, while bone formation is not suppressed by this therapy.