Mok Chi Chiu, Ho Ling Yin, Ma Kwok Man
Department of Medicine, Tuen Mun Hospital, Hong Kong.
Department of Medicine, Tuen Mun Hospital, Hong Kong.
Bone. 2015 Jun;75:222-8. doi: 10.1016/j.bone.2015.03.002. Epub 2015 Mar 8.
To evaluate the effect of switching from oral bisphosphonates to denosumab on bone mineral density (BMD) in long-term glucocorticoid users.
Adult patients who were receiving long-term prednisolone (≥2.5 mg/day for ≥1 year) and oral bisphosphonates (≥2 years) were recruited. Participants were randomized to either continue oral bisphosphonates or switch to denosumab (60 mg subcutaneously every 6 months) for 12 months. Serial BMD (lumbar spine, hip) and bone turnover markers (serum osteocalcin, P1NP, β-CTX) were measured.
42 women were recruited (age 54.7±12.9 years; 21 shifted to denosumab and 21 continued on bisphosphonates). The duration of prednisolone therapy was 101±66.3 months and the daily dose was 4.4±2.1 mg. Baseline demographic data, osteoporosis risk factors, and BMD at various sites were similar between the two groups of patients. At month 12, BMD of the spine and hip increased by +3.4±0.9% (p=0.002) and +1.4±0.6% (p=0.03), respectively, in the denosumab group; whereas the corresponding change was +1.5±0.4% (p=0.001) and +0.80±0.5% (p=0.12) in the bisphosphonate group. The spinal BMD at month 12 was significantly higher in the denosumab than bisphosphonate group after adjustment for baseline BMD and β-CTX values, and other confounding factors (p=0.01). Bone turnover markers (β-CTX and P1NP) were more strongly suppressed by denosumab than the bisphosphonates. Minor infections were more common in denosumab-treated patients while other adverse events occurred at similar frequencies between the two groups.
In patients receiving long-term glucocorticoids, switching from oral bisphosphonates to denosumab resulted in greater gain of the spinal BMD and suppression of bone turnover markers after 12 months of therapy. The results have to be confirmed by a larger clinical trial with fracture as endpoint.
评估长期使用糖皮质激素的患者从口服双膦酸盐转换为地诺单抗对骨密度（BMD）的影响。
招募接受长期泼尼松龙治疗（≥2.5毫克/天，持续≥1年）且口服双膦酸盐（≥2年）的成年患者。参与者被随机分为继续口服双膦酸盐或转换为地诺单抗（每6个月皮下注射60毫克）治疗12个月。测量系列骨密度（腰椎、髋部）和骨转换标志物（血清骨钙素、I型前胶原氨基端前肽、β-胶原降解产物）。
招募了42名女性（年龄54.7±12.9岁；21名转换为地诺单抗，21名继续使用双膦酸盐）。泼尼松龙治疗的持续时间为101±66.3个月，每日剂量为4.4±2.1毫克。两组患者的基线人口统计学数据、骨质疏松风险因素以及各部位的骨密度相似。在第12个月时，地诺单抗组脊柱和髋部的骨密度分别增加了+3.4±0.9%（p=0.002）和+1.4±0.6%（p=0.03）；而双膦酸盐组相应的变化为+1.5±0.4%（p=0.001）和+0.80±0.5%（p=0.12）。在调整基线骨密度和β-胶原降解产物值以及其他混杂因素后，地诺单抗组第12个月时的脊柱骨密度显著高于双膦酸盐组（p=0.01）。地诺单抗比双膦酸盐更能强烈抑制骨转换标志物（β-胶原降解产物和I型前胶原氨基端前肽）。地诺单抗治疗的患者中轻微感染更为常见，而两组其他不良事件的发生频率相似。
在接受长期糖皮质激素治疗的患者中，从口服双膦酸盐转换为地诺单抗在治疗12个月后可使脊柱骨密度有更大增加，并抑制骨转换标志物。结果有待以骨折为终点的更大规模临床试验进行证实。
