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糖皮质激素性骨质疏松症:从基础机制到临床层面

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

作者信息

Alesci Salvatore, De Martino Massimo U, Ilias Ioannis, Gold Philip W, Chrousos George P

机构信息

Clinical Neuroendocrinology Branch, National Institute of Mental Health, Bethesda, MD 20892-1284, USA.

出版信息

Neuroimmunomodulation. 2005;12(1):1-19. doi: 10.1159/000082360.

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.

摘要

糖皮质激素(GC)诱导的骨质疏松症(GCOP)是20至45岁成年人骨质疏松症最常见的病因,也是医源性骨质疏松症最常见的病因。内源性或外源性GC过量在30%至50%的病例中会导致骨质流失。实际上,导致骨折的骨质流失可能是GC治疗最使人丧失能力的并发症,有时部分不可逆。然而,GCOP常常诊断不足且未得到治疗。以下文章提供了有关GC诱导的骨质流失病理生理学所涉及的细胞和分子机制的最新信息,以及针对这种病症的诊断、预防和治疗策略的一些指南,以促进患者和医生对GCOP有更好的了解和更高的认识。

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