Yamauchi Mika
Internal Medicine 1, Shimane University Faculty of Medicine.
Clin Calcium. 2009 Aug;19(8):1092-1100.
Bone mineral density (BMD) is not sensitive enough to assess the bone strength especially in patients treated with glucocorticoid (GC) . GC therapy induces deterioration of bone quality. The measurements of biochemical bone markers which can be measured in medical practice in Japan are the useful tool for assessing the bone quality. Our study revealed that urinary deoxypyridinoline level was a BMD-independent marker for prevalent vertebral fractures in GC-treated postmenopausal women. Administration of high dose of GC causes an immediate decrease in bone formation followed by a rapid and transient increase in bone resorption. In patients receiving high dose of GC, there were uncoupling between bone formation and bone resorption which causes bone loss as well as bone fragility. In patients with GC treatment, bisphosphonate is effective in decreasing bone resorption marker. The suppression of bone resorption by bisphosphonate inhibits bone loss and deterioration of bone strength in GIO.
骨密度（BMD）对于评估骨强度不够敏感，尤其是在接受糖皮质激素（GC）治疗的患者中。GC治疗会导致骨质量恶化。在日本医疗实践中可测量的生化骨标志物是评估骨质量的有用工具。我们的研究表明，尿脱氧吡啶啉水平是接受GC治疗的绝经后女性中既往椎体骨折的一个与BMD无关的标志物。高剂量GC给药会立即导致骨形成减少，随后骨吸收迅速短暂增加。在接受高剂量GC的患者中，骨形成与骨吸收之间存在解偶联，这会导致骨质流失以及骨脆性增加。在接受GC治疗的患者中，双膦酸盐可有效降低骨吸收标志物。双膦酸盐对骨吸收的抑制作用可抑制糖皮质激素性骨质疏松症（GIO）中的骨质流失和骨强度恶化。
