CHANGES IN (MARKERS OF) BONE METABOLISM DURING HIGH-DOSE CORTICOSTEROID PULSE TREATMENT IN PATIENTS WITH RHEUMATOID-ARTHRITIS

Citation
Wf. Lems et al., CHANGES IN (MARKERS OF) BONE METABOLISM DURING HIGH-DOSE CORTICOSTEROID PULSE TREATMENT IN PATIENTS WITH RHEUMATOID-ARTHRITIS, Annals of the Rheumatic Diseases, 55(5), 1996, pp. 288-293
Citations number
38
Categorie Soggetti
Rheumatology
ISSN journal
00034967
Volume
55
Issue
5
Year of publication
1996
Pages
288 - 293
Database
ISI
SICI code
0003-4967(1996)55:5<288:CI(OBM>2.0.ZU;2-F
Abstract
Objective-To examine the effect of high dose corticosteroid pulse trea tment (three times 200 mg dexamethasone intravenously in eight days) o n calcium and bone metabolism in 17 consecutive patients with active r heumatoid arthritis (RA). Methods-Bone formation was quantified by mea surement of serum alkaline phosphatase, osteocalcin, and carboxytermin al propeptide of type I procollagen (pro-I-CPP) concentrations. Bone r esorption was measured by urinary excretion of calcium, hydroxyproline , (free and total) pyridinoline (Pyr), and serum concentrations of the carboxyterminal cross linked telopeptide of type I collagen (I-CTP). Disease activity of RA was measured by erythrocyte sedimentation rate, C reactive protein, and Ritchie and Thompson joint scores. Results-Di sease activity was initially high, and decreased during corticosteroid pulse treatment and the following five weeks. Osteocalcin, alkaline p hosphatase, and pro-I-CPP concentrations were initially within normal limits, while I-CTP, Dpyr, and Pyr were increased. Osteocalcin and pro -I-CPP concentrations decreased (p<0.01) during corticosteroid pulse t reatment, but rapidly returned to baseline after the treatment. No cha nges were observed in alkaline phosphatase and urinary excretion of ca lcium and hydroxyproline. Bone resorption measured by serum I-CTP and urinary excretion of Pyr and Dpyr was unchanged or decreased (p<0.05-0 .01), depending on the time of measurement and the parameter measured. Conclusions-In these patients with active RA, bone resorption was inc reased, while bone formation was within normal limits. During high dos e corticosteroid pulse treatment, bone formation was only transiently decreased, while markers of bone resorption were unchanged or decrease d. Because corticosteroid pulse treatment has only a short term negati ve effect on bone formation, and because it probably reduces bone reso rption, at least partly as a result of the decreased disease activity, the effect of corticosteroid pulse treatment on bone may be assumed t o be relatively mild.