Ashcroft Andrew J, Davies Faith E, Morgan Gareth J
Epidemiology and Genetics Unit, University of Leeds, UK.
Lancet Oncol. 2003 May;4(5):284-92. doi: 10.1016/s1470-2045(03)01076-3.
Osteolytic bone disease is a major cause of morbidity in patients with multiple myeloma. Our understanding of the pathophysiology of multiple myeloma has increased substantially during the past decade. However the underlying mechanisms of bone destruction and the treatments available have, until recently, received relatively little specific attention. In this review, we provide an overview of the RANK/RANKL/osteoprotegerin system; we describe its interaction with other cellular mechanisms, through which malignant plasma cells drive osteolysis, and explain how bisphosphonates can be used to block this action. We also review the supporting evidence for bisphosphonates as the treatment of choice for patients with bone complications related to multiple myeloma, and discuss possible developments for targeted therapy in the future.
溶骨性骨病是多发性骨髓瘤患者发病的主要原因。在过去十年中，我们对多发性骨髓瘤病理生理学的认识有了显著提高。然而，直到最近，骨破坏的潜在机制和可用的治疗方法相对来说受到的具体关注较少。在这篇综述中，我们概述了RANK/RANKL/骨保护素系统；我们描述了它与其他细胞机制的相互作用，恶性浆细胞通过这些机制驱动骨溶解，并解释了双膦酸盐如何用于阻断这种作用。我们还回顾了双膦酸盐作为多发性骨髓瘤相关骨并发症患者首选治疗方法的支持证据，并讨论了未来靶向治疗的可能发展。
