Erschienen in:
01.09.2008 | Consensus Statement
Recommendations for the registration of agents for prevention and treatment of glucocorticoid-induced osteoporosis: an update from the Group for the Respect of Ethics and Excellence in Science
verfasst von:
J. Compston, D. M. Reid, J. Boisdron, M.-L. Brandi, N. Burlet, D. Cahall, P. D. Delmas, W. Dere, J.-P. Devogelaer, L. A. Fitzpatrick, B. Flamion, N. Goel, S. Korte, A. Laslop, B. Mitlak, S. Ormarsdottir, J. Ringe, R. Rizzoli, Y. Tsouderos, T. Van Staa, J.-Y. Reginster
Erschienen in:
Osteoporosis International
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Ausgabe 9/2008
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Excerpt
Oral glucocorticoid therapy is widely used for the treatment of a variety of diseases. Approximately 1% of the population is prescribed oral glucocorticoids, and in the elderly this prevalence rises to 2.5% [
1]. The association between glucocorticoid therapy and osteoporosis is well documented and exhibits some characteristic features [
2]. Bone loss is particularly rapid in the first few months after initiation of therapy, with a slower rate of loss subsequently [
3]. Fracture risk also increases rapidly during the early months of therapy and declines after its cessation [
4,
5]. Both cortical and cancellous bone are affected, and there is some reversibility of bone loss after cessation or reduction of therapy [
3,
6]. Although the severity of osteoporosis is related to the dose and duration of glucocorticoid therapy, some increase in fracture risk is seen even at daily doses of ≤7.5 mg daily for 3–6 months [
4,
5]. Finally, the effect of glucocorticoids on bone fragility is, to some extent, independent of bone mineral density, fractures occurring at a higher bone mineral density (BMD) threshold than in postmenopausal osteoporosis (PMO) [
7‐
9]. …