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Osteoporosis in rheumatoid arthritis--significance of alfacalcidol in prevention and therapy

Schacht E

Zeitschrift fur Rheumatologie, 2000

Abstract

Besides localised osteopenia, patients with rheumatoid arthritis (RA) with or without corticosteroids develop in 30-50% osteoporosis induced by several factors and thus a higher risk of fractures. Bone loss appears very early and correlates directly with disease activity and also later with the negative effects of restrictive mobility. Corticosteroids reduce as a pathogenetic co-factor intestinal calcium absorption and increase renal calcium excretion resulting in compensatory increased PTH-release and increased sensitivity of bone to PTH. In addition, corticosteroids inhibit osteoblast function as well as the favourable effects of growth factors and sex hormones on bone. It has recently been recognised that the expression of D-hormone receptors (VDRs) is suppressed by these medications and that corticosteroids probably induce VDR disorders. The negative influence of corticosteroids on muscle strength (indirectly--via increased PTH-levels, lowered IGF-1-levels or reduced D-hormone activity) is a feature which has been underestimated. The demonstrated drop in 1,25(OH)2D3 (D-hormone) levels in patients with RA in correlation with C-reactive protein (CRP) is of significance in the pathogenesis of RA-induced osteoporosis and could further promote the process of inflammation. There is a general consensus that cytokines (e.g. IL-1, IL-6, IL-12, TNF-alpha) induce bone resorption in inflammatory rheumatic diseases. There are, however, new findings which show that cytokines like…

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