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The course of biochemical parameters of bone turnover during treatment with corticosteroids
M F Prummel1, W M Wiersinga, P Lips
1Department of Endocrinology, University of Amsterdam, The Netherlands.
Abstract:
The mechanisms by which glucocorticoids cause osteopenia are incompletely understood. It is generally accepted that bone formation is depressed during corticosteroid treatment, but the cause of the ongoing bone resorption is less clear. Secondary hyperparathyroidism and changes in vitamin D metabolism are thought to play a role. This is based mostly on data from cross-sectional studies in heterogeneous patient groups. We, therefore, studied longitudinally the course of biochemical parameters and the hormones influencing bone turnover in a homogeneous group of 10 euthyroid patients with Graves' ophthalmopathy, all euthyroid for at least 1 yr before, during, and after a 12-week course of prednisone. Bone formation was depressed as reflected by a fall in serum osteocalcin (3.0 +/- 2.1, 1.7 +/- 1.1, and 2.4 +/- 1.9 micrograms/L at weeks 0, 4, and 12, respectively; P = 0.02) and in total alkaline phosphatase (1.15 +/- 0.33, 0.83 +/- 0.22, and 0.88 +/- 0.40 mukat/L; P = 0.001). Parameters of bone resorption (urinary hydroxyproline/creatinine ratio, serum acid phosphatase) and the levels of vitamin D metabolites remained unchanged. Serum intact PTH seemed to decrease slightly. Our findings suggest that glucocorticoid induced osteopenia is caused by a depressed bone formation in the presence of an unaltered but ongoing bone resorption. Secondary hyperparathyroidism and changes in vitamin D metabolism are apparently not involved.
Insights
Glucocorticoids depress bone formation, leading to osteopenia. This study found that bone resorption remains unchanged, ruling out secondary hyperparathyroidism or vitamin D changes as causes.
Area of Science:
- Endocrinology
- Bone Metabolism
- Pharmacology
Background:
- Glucocorticoids are known to cause osteopenia.
- The exact mechanisms, particularly regarding bone resorption, are not fully understood.
- Previous studies relied on heterogeneous patient groups and cross-sectional data.
Purpose of the Study:
- To longitudinally investigate the biochemical markers of bone turnover during glucocorticoid treatment.
- To clarify the role of secondary hyperparathyroidism and vitamin D metabolism in glucocorticoid-induced osteopenia.
Main Methods:
- A longitudinal study of 10 euthyroid patients with Graves' ophthalmopathy.
- Patients received a 12-week course of prednisone.
- Biochemical parameters of bone formation and resorption, vitamin D metabolites, and parathyroid hormone were measured before, during, and after treatment.
Main Results:
- Prednisone significantly decreased markers of bone formation (serum osteocalcin and total alkaline phosphatase).
- Markers of bone resorption (urinary hydroxyproline/creatinine ratio, serum acid phosphatase) remained unchanged.
- Vitamin D metabolites and serum intact parathyroid hormone levels showed no significant changes.
Conclusions:
- Glucocorticoid-induced osteopenia is primarily due to depressed bone formation.
- Ongoing bone resorption is not significantly altered by glucocorticoid treatment in this context.
- Secondary hyperparathyroidism and altered vitamin D metabolism do not appear to be involved mechanisms.