Glucocorticoid-induced osteoporosis and parathyroid hormone.

R. Carpinteri, T. Porcelli, C. Mejia, I. Patelli, J. P. Bilezikian, E. Canalis, A. Angeli, A. Giustina, G. Mazziotti

Résultat de rechercheexamen par les pairs

26 Citations (Scopus)

Résumé

Glucocorticoid-induced osteoporosis (GIO) is the most common form of secondary osteoporosis. Bisphosphonates are considered the first-line treatment option for the majority of glucocorticoid-treated patients at increased risk of fractures. However, the anti-resorptive mechanism of bisphosphonates does not address the major pathophysiological mechanisms of impaired bone formation during chronic glucocorticoid treatment. PTH, when administered intermittently and at low doses, has effects on bone formation opposite to those of glucocorticoids and therefore is conceptually a more attractive approach. Teriparatide (1-34PTH) has been studied in patients with GIO with effects on bone mineral density and on fracture risk which were shown to be superior to those obtained with alendronate.

Langue d'origineEnglish
Pages (de-à)16-21
Nombre de pages6
JournalJournal of Endocrinological Investigation
Volume33
Numéro de publication7 Suppl
Statut de publicationPublished - 2010

Financement

Bailleurs de fondsNuméro du bailleur de fonds
National Institute of Diabetes and Digestive and Kidney DiseasesR01DK032333

    ASJC Scopus Subject Areas

    • Endocrinology, Diabetes and Metabolism
    • Endocrinology

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