CHU Brugmann, Université Libre de Bruxelles, Brussels, Belgium.
BMC Cancer. 2011 Aug 29;11:384. doi: 10.1186/1471-2407-11-384.
Women with breast cancer, particularly individuals diagnosed at a relatively early age, have an increased incidence of fractures. Fractures can have serious clinical consequences including the need for major surgery, increased morbidity and mortality, increased cost of disease management, and reduced quality of life for patients. The primary cause of the increased fracture risk appears to be an accelerated decrease in bone mineral density (BMD) resulting from the loss of estrogenic signaling that occurs with most treatments for breast cancer, including aromatase inhibitors. However, factors other than BMD levels alone may influence treatment decisions to reduce fracture risk in this setting. Our purpose is to review current evidence for BMD loss and fracture risk during treatment for breast cancer and discuss pharmacologic means to reduce this risk.
Fracture risk during treatment for breast cancer may be influenced by the rate of BMD loss and the consequent rapid alterations in bone microarchitecture, in addition to the established fracture risk factors in postmenopausal osteoporosis. The rapid decrease in BMD during adjuvant chemoendocrine therapy for breast cancer may necessitate more aggressive pharmacotherapy than is indicated for healthy postmenopausal women who develop osteoporosis. Over the last few years, clinical trials have established the effectiveness of bisphosphonates and other antiresorptive agents to preserve BMD during adjuvant therapy for early breast cancer. In addition, some bisphosphonates (eg, zoledronic acid) may also delay disease recurrence in women with hormone-responsive tumors, thereby providing an adjuvant benefit in addition to preserving BMD and potentially preventing fractures.
It is likely that a combined fracture risk assessment (eg, as in the WHO FRAX algorithm) will more accurately identify both women with postmenopausal osteoporosis and women with breast cancer who require bone-protective therapy.
患有乳腺癌的女性，尤其是那些相对较早被诊断出患有乳腺癌的女性，骨折的发病率更高。骨折会产生严重的临床后果，包括需要进行重大手术、发病率和死亡率增加、疾病管理成本增加以及患者生活质量下降。骨折风险增加的主要原因似乎是由于大多数乳腺癌治疗方法（包括芳香酶抑制剂）导致雌激素信号丢失，从而导致骨密度（BMD）加速下降。然而，除了 BMD 水平之外，其他因素也可能影响降低这种情况下骨折风险的治疗决策。我们的目的是回顾乳腺癌治疗期间 BMD 丢失和骨折风险的现有证据，并讨论降低这种风险的药物治疗方法。
乳腺癌治疗期间的骨折风险可能受到 BMD 丢失率和随之而来的骨微观结构快速变化的影响，除了绝经后骨质疏松症中已确立的骨折危险因素之外。乳腺癌辅助化疗内分泌治疗期间 BMD 的快速下降可能需要比健康绝经后妇女发生骨质疏松症时更积极的药物治疗。在过去的几年中，临床试验已经确定了双膦酸盐和其他抗吸收剂在早期乳腺癌辅助治疗中维持 BMD 的有效性。此外，一些双膦酸盐（如唑来膦酸）还可能延迟激素反应性肿瘤女性的疾病复发，从而除了维持 BMD 并可能预防骨折外，还提供辅助益处。
联合骨折风险评估（例如，在世界卫生组织 FRAX 算法中）可能更准确地识别绝经后骨质疏松症和需要骨保护治疗的乳腺癌女性。
