Neuroendocrine Unit, Massachusetts General Hospital, Boston, Massachusetts, USA.
Harvard Medical School, Boston, Massachusetts, USA.
Eur J Endocrinol. 2022 Oct 13;187(5):697-708. doi: 10.1530/EJE-22-0248. Print 2022 Nov 1.
Anorexia nervosa is complicated by high bone resorption, low bone mineral density (BMD), and increased fracture risk. We investigated whether off-label antiresorptive therapy with denosumab increases BMD in women with anorexia nervosa.
Twelve-month, randomized, double-blind, placebo-controlled study.
Thirty ambulatory women with anorexia nervosa and areal BMD (aBMD) T-score <-1.0 at ≥1 sites were randomized to 12 months of denosumab (60 mg subcutaneously q6 months)(n = 20) or placebo (n = 10). Primary end point was postero-anterior (PA) lumbar spine aBMD by dual-energy x-ray absorptiometry. Secondary end points included femoral neck aBMD, tibia and radius volumetric BMD and bone microarchitecture by high-resolution peripheral quantitative CT, tibia and radius failure load by finite element analysis (FEA), and markers of bone turnover.
Baseline mean (±s.d.) age (29 ± 8 (denosumab) vs 29 ± 7 years (placebo)), BMI (19.0 ± 1.7 vs 18.0 ± 2.0 kg/m2), and aBMD (PA spine Z-score -1.6±1.1 vs -1.7±1.4) were similar between groups. PA lumbar spine aBMD increased in the denosumab vs placebo group over 12 months (P = 0.009). The mean (95% CI) increase in PA lumbar spine aBMD was 5.5 (3.8-7.2)% in the denosumab group and 2.2 (-0.3-4.7)% in the placebo group. The change in femoral neck aBMD was similar between groups. Radial trabecular number increased, radial trabecular separation decreased, and tibial cortical porosity decreased in the denosumab vs placebo group (P ≤ 0.006). Serum C-terminal telopeptide of type I collagen and procollagen type I N-terminal propeptide decreased in the denosumab vs placebo group (P < 0.0001). Denosumab was well tolerated.
Twelve months of antiresorptive therapy with denosumab reduced bone turnover and increased spine aBMD, the skeletal site most severely affected in women with anorexia nervosa.
神经性厌食症伴有骨吸收增加、骨密度降低(BMD)和骨折风险增加。本研究旨在探讨抗吸收药物地舒单抗能否增加神经性厌食症女性的 BMD。
12 个月、随机、双盲、安慰剂对照研究。
30 例门诊神经性厌食症患者,至少 1 个部位的 BMD (aBMD) T 评分<-1.0,随机分为地舒单抗(60 mg 皮下每 6 个月一次)(n=20)或安慰剂(n=10)12 个月。主要终点是双能 X 线吸收法测定的前后位(PA)腰椎 aBMD。次要终点包括股骨颈 aBMD、胫骨和桡骨体积 BMD 和骨微结构的高分辨率外周定量 CT、胫骨和桡骨失效负荷的有限元分析(FEA)以及骨转换标志物。
基线时(±标准差)年龄(地舒单抗组 29 ± 8 岁,安慰剂组 29 ± 7 岁)、BMI(地舒单抗组 19.0 ± 1.7 kg/m2,安慰剂组 18.0 ± 2.0 kg/m2)和 aBMD(PA 脊柱 Z 评分-1.6±1.1,-1.7±1.4)在两组间相似。地舒单抗组与安慰剂组相比,PA 腰椎 aBMD 在 12 个月内增加(P=0.009)。地舒单抗组 PA 腰椎 aBMD 平均(95%CI)增加 5.5(3.8-7.2)%,安慰剂组增加 2.2(-0.3-4.7)%。两组间股骨颈 aBMD 变化相似。地舒单抗组桡骨小梁数量增加,桡骨小梁分离减少,胫骨皮质孔隙度降低(P ≤ 0.006)。地舒单抗组血清Ⅰ型胶原 C 端肽和Ⅰ型前胶原 N 端前肽减少(P<0.0001)。地舒单抗耐受性良好。
抗吸收药物地舒单抗治疗 12 个月可降低骨转换并增加脊柱 aBMD,这是神经性厌食症女性最严重的骨骼部位。