Glucocorticoid-induced osteoporosis: 2013 update
| Autor: | M. Mazzantini, O. Di Munno |
|---|---|
| Jazyk: | English<br />Italian |
| Rok vydání: | 2014 |
| Předmět: | |
| Zdroj: | Reumatismo, Vol 66, Iss 2, Pp 144-152 (2014) |
| Druh dokumentu: | article |
| ISSN: | 0048-7449 2240-2683 |
| DOI: | 10.4081/reumatismo.2014.787 |
| Popis: | Glucocorticoids are the most common cause of secondary osteoporosis leading to the so-called glucocorticoidinduced osteoporosis (GIO). A treatment with 10 mg/d of prednisone or equivalent for more than 3 months leads to a 7-fold increase in hip fractures and a 17-fold increase in vertebral fractures. The difference between bone quantity and quality in GIO makes bone mineral density measurements inadequate to detect patients at risk of fracture. The adverse effects of glucocorticoids on the skeleton derive from a direct impact on bone cells with a severe impairment of mechanical competence. Crucial to prevention of GIO is early timing of intervention. The World Health Organization has adopted a fracture prevention algorithm (FRAX) intended to estimate fracture risk in GIO. The American College of Rhematology modified its prevention and treatment guidelines taking into account the individual risk of fracture calculated in GIO on the basis of the FRAX algorithm. Recently, also a joint Guideline Working Group of the International Osteoporosis Foundation (IOF) and the European Calcified Tissue Society (ECTS) published a framework for the development of national guidelines for the management of GIO. Bisphosphonates are the first-line drugs to treat GIO; teriparatide counteracts several fundamental pathophysiologic aspects of GIO; denosumab is useful in patients with renal failure and in potentially pregnant young women. Vertebroplasty and kyphoplasty may be less beneficial in GIO than in primary involutional osteoporosis. |
| Databáze: | Directory of Open Access Journals |
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