Compston Juliet
Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge, UK.
Horm Res. 2003;60 Suppl 3:77-9. doi: 10.1159/000074506.
Osteoporosis is a common and serious complication of glucocorticoid therapy, resulting in increased risk of fragility fractures. Recent studies indicate that fracture risk is increased even at low doses of glucocorticoids and that this increased risk is seen soon after the commencement of glucocorticoid therapy. Both increased bone resorption and reduced bone formation contribute to bone loss, which affects cortical and cancellous sites. A number of interventions have been shown to prevent glucocorticoid-induced bone loss, although the strongest evidence exists for the bisphosphonates etidronate, alendronate and risedronate. Primary prevention of bone loss should be considered in all high-risk individuals taking oral glucocorticoids for 3 months or more, for example those aged 65 years or over or those with a previous fragility fracture. In other glucocorticoid-treated individuals, the decision to treat should be based on bone densitometry.
骨质疏松症是糖皮质激素治疗常见且严重的并发症,会导致脆性骨折风险增加。近期研究表明,即使使用低剂量糖皮质激素,骨折风险也会增加,且在糖皮质激素治疗开始后不久就能观察到这种风险增加。骨吸收增加和骨形成减少均会导致骨质流失,这会影响皮质骨和松质骨部位。尽管双膦酸盐类药物依替膦酸二钠、阿仑膦酸钠和利塞膦酸钠有最有力的证据支持,但已证明多种干预措施可预防糖皮质激素诱发的骨质流失。对于所有口服糖皮质激素3个月及以上的高危个体,例如65岁及以上者或既往有脆性骨折者,应考虑对骨质流失进行一级预防。在其他接受糖皮质激素治疗的个体中,治疗决策应基于骨密度测定结果。