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      Call for Papers: Epidemiology and Health Impacts of Neuroendocrine Tumors

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      About Neuroendocrinology: 3.2 Impact Factor I 8.3 CiteScore I 1.009 Scimago Journal & Country Rank (SJR)

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      Glucocorticoid-induced osteoporosis: from basic mechanisms to clinical aspects.

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          Abstract

          Glucocorticoid (GC)-induced osteoporosis (GCOP) is the most common cause of osteoporosis in adults aged 20-45 years as well as the most common cause of iatrogenic osteoporosis. GC excess, either endogenous or exogenous, induces bone loss in 30-50% of cases. Indeed, bone loss leading to fractures is perhaps the most incapacitating, sometimes partially irreversible, complication of GC therapy. Nevertheless, GCOP is often underdiagnosed and left untreated. The following article provides an update on the cellular and molecular mechanisms implicated in the pathophysiology of GC-induced bone loss, as well as some guidelines on diagnostic, preventive and therapeutic strategies for this medical condition, in an effort to promote a better knowledge and greater awareness of GCOP by both the patient and the physician.

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          Most cited references158

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          Consensus development conference: diagnosis, prophylaxis, and treatment of osteoporosis.

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            Birth and Death of Bone Cells: Basic Regulatory Mechanisms and Implications for the Pathogenesis and Treatment of Osteoporosis

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              Nontraumatic necrosis of bone (osteonecrosis).

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                Author and article information

                Journal
                Neuroimmunomodulation
                Neuroimmunomodulation
                1021-7401
                1021-7401
                2005
                : 12
                : 1
                Affiliations
                [1 ] Clinical Neuroendocrinology Branch, National Institute of Mental Health, Bethesda, MD 20892-1284, USA. alescisa@mail.nih.gov
                Article
                82360
                10.1159/000082360
                15756049
                9d7d92bf-d7a6-49c8-968e-b5ad1b58a84e
                History

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