The University of Alabama at Birmingham.
Amgen Inc., Thousand Oaks, California.
Arthritis Rheumatol. 2022 Apr;74(4):604-611. doi: 10.1002/art.41981. Epub 2022 Feb 13.
To evaluate changes in bone turnover and bone mineral density (BMD) in patients with rheumatoid arthritis (RA) receiving glucocorticoids, after discontinuation of denosumab for 12 months.
We conducted a randomized, double-blind, placebo-controlled, phase II study of RA patients. Patients received placebo, denosumab 60 mg, or denosumab 180 mg every 6 months for 12 months and were followed up for an additional 12 months after discontinuation, during which no bone loss prevention therapy was instituted. Changes from baseline in serum C-terminal telopeptide of type I collagen (CTX), serum procollagen type I N-terminal propeptide (PINP), and lumbar spine and total hip BMD were evaluated.
In this post hoc analysis of patients treated with glucocorticoids at study baseline (n = 82), levels of CTX and PINP decreased significantly from baseline in both denosumab groups. Following denosumab discontinuation, CTX returned to baseline and was not significantly different from the placebo group 6 and 12 months after discontinuation. Median percentage changes from baseline PINP in those treated with denosumab 60 mg were -0.16% and 15.3% at 6 and 12 months, respectively, after discontinuation (P = 0.062 and P = 0.017, versus placebo); corresponding changes with denosumab 180 mg were 9.0% and 75.8%, respectively (P = 0.018 and P = 0.002 versus placebo). Compared to placebo, lumbar spine and total hip BMD increased in patients receiving denosumab and returned to baseline 12 months after discontinuation. No osteoporotic fractures were reported during treatment or in the off-treatment period.
In this analysis of short-term denosumab use in RA patients receiving glucocorticoids, denosumab discontinuation resulted in a gradual increase in bone turnover, which was associated with a return to baseline lumbar spine and total hip BMD.
评估停用地舒单抗 12 个月后，接受糖皮质激素治疗的类风湿关节炎（RA）患者的骨转换和骨密度（BMD）变化。
我们开展了一项 RA 患者的随机、双盲、安慰剂对照、II 期研究。患者接受安慰剂、地舒单抗 60mg 或地舒单抗 180mg，每 6 个月 1 次，共 12 个月，停药后随访 12 个月，期间未进行任何预防骨质流失治疗。评估血清 I 型胶原 C 端肽（CTX）、血清 I 型前胶原 N 端前肽（PINP）以及腰椎和全髋 BMD 自基线的变化。
在本项研究中，根据基线时接受糖皮质激素治疗的患者（n=82）进行的事后分析中，CTX 和 PINP 水平在两组地舒单抗治疗患者中均自基线显著下降。地舒单抗停药后，CTX 恢复至基线水平，停药后 6 和 12 个月与安慰剂组无显著差异。接受地舒单抗 60mg 治疗者的基线 PINP 中位数百分比变化分别为停药后 6 和 12 个月时为-0.16%和 15.3%（P=0.062 和 P=0.017，与安慰剂相比）；接受地舒单抗 180mg 治疗者的相应变化分别为 9.0%和 75.8%（P=0.018 和 P=0.002，与安慰剂相比）。与安慰剂相比，接受地舒单抗治疗的患者的腰椎和全髋 BMD 增加，并在停药后 12 个月恢复至基线。治疗期间或停药期间均未报告骨质疏松性骨折。
在这项 RA 患者短期使用地舒单抗的分析中，停用地舒单抗后骨转换逐渐增加，与腰椎和全髋 BMD 恢复至基线相关。
