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Rheumatology 2000; 39: 523-529
© 2000 British Society for Rheumatology

Acute effects of etidronate on glucocorticoid-induced bone degradation

A. Struijs, A. Smals1, S. A. de Witte, W. H. L. Hackeng2 and H. Mulder3

Department of Internal Medicine and Endocrinology, University Hospital ‘Dijkzigt’, Dr Molenwaterplein 40, 3015 GD Rotterdam,
1 Division of Endocrinology, Department of Internal Medicine, University Hospital St Radboud, Nijmegen,
2 Praktijk voor Laboratorium Diagnostiek, Spijkenisse and
3 Site Management Organisation, ‘Good Clinical Practice’, Walenburgerweg 33, 3039 AC Rotterdam, The Netherlands

Objectives. To study the acute short-term effects on the biochemical parameters of calcium and bone homeostasis in post-menopausal women treated with a high dose of prednisone alone or with additional etidronate, before and during 5 days of treatment.

Methods. Serum calcium, phosphorus, creatinine, alkaline phosphatase activity, osteocalcin, carboxy-terminal propeptide of type I procollagen (PICP), cross-linked carboxy-terminal telopeptide of type I collagen (ICTP), parathyroid hormone (PTH), 25-hydroxyvitamin D and urinary excretion of calcium over 24 h were measured before and during 5 days of treatment in 14 post-menopausal women treated with a high dose of prednisone (60 mg/day) alone (group A) or combined with cyclical etidronate (group B).

Results. Significant differences from baseline were found in osteocalcin and urinary excretion of calcium in both groups and for ICTP in group B. Significant differences between groups were calculated at day 5 of the study for osteocalcin, ICTP and 24 h urine calcium excretion (P < 0.01). Urinary excretion of calcium over 24 h increased in group A (+14.7%; P < 0.05) and decreased in group B (-22.1%; P < 0.01). Osteocalcin levels decreased in group A (- 38.1%) and increased in group B (+27.4%; both P < 0.01). ICTP decreased only in group B (-19.4%; P < 0.01).

Conclusions. The results are consistent with the fact that etidronate is acutely able to prevent bone resorption due to corticosteroids. The increase in osteocalcin in the etidronate-treated group is a new feature. A direct or indirect (PTH, 1,25 vitamin D?) stimulatory effect of etidronate on the osteoblast cannot be excluded.

KEY WORDS: Prednisone, Corticosteroid, Glucocorticoid, Etidronate, Bisphosphonate, Osteoporosis, Calcium metabolism, Bone markers.

Correspondence to: A. Struijs, Noordenstraat 3, 2921 AK Krimpen, Yssel, The Netherlands.


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