The Mellanby Centre for Bone Research, Department of Oncology and Metabolism, The University of Sheffield, Sheffield, United Kingdom.
Metabolic Bone Centre, Sheffield Teaching Hospitals National Health Service Foundation Trust, Sheffield, United Kingdom.
J Clin Endocrinol Metab. 2018 Apr 1;103(4):1302-1309. doi: 10.1210/jc.2017-00283.
Treatment of postmenopausal osteoporosis with teriparatide parathyroid hormone amino terminal 1-34 increases bone formation and improves bone microarchitecture. A possible modulator of action is periostin. In vitro experiments have shown that periostin might regulate osteoblast differentiation and bone formation through Wnt signaling. The effect of teriparatide on periostin is not currently known.
To determine the effect of teriparatide treatment on circulating levels of periostin and other regulators of bone formation and investigate how changes in periostin relate to changes in bone turnover markers, regulators of bone formation, and bone mineral density (BMD).
Twenty women with osteoporosis; a 2-year open-label single-arm study.
Teriparatide 20 µg was administered by subcutaneous injection daily for 104 weeks. Periostin, sclerostin, and Dickkopf-related protein 1, procollagen type I N-terminal propeptide (PINP), and C-telopeptide of type I collagen were measured in fasting serum collected at baseline (two visits) and then at weeks 1, 2, 4, 12, 26, 52, 78, and 104. BMD was measured at the lumbar spine, total hip, and femoral neck using dual energy x-ray absorptiometry.
Periostin levels increased by 6.6% [95% confidence interval (CI), -0.4 to 13.5] after 26 weeks of teriparatide treatment and significantly by 12.5% (95% CI, 3.3 to 21.0; P < 0.01) after 52 weeks. The change in periostin correlated positively with the change in the lumbar spine BMD at week 52 (r = 0.567; 95% CI, 0.137 to 0.817; P < 0.05) and femoral neck BMD at week 104 (r = 0.682; 95% CI, 0.261 to 0.885; P < 0.01).
Teriparatide therapy increases periostin secretion; it is unclear whether this increase mediates the effect of the drug on bone.
甲状旁腺激素氨基端 1-34（特立帕肽）治疗绝经后骨质疏松症可增加骨形成并改善骨微结构。一种可能的作用调节剂是骨膜蛋白。体外实验表明，骨膜蛋白可能通过 Wnt 信号调节成骨细胞分化和骨形成。目前尚不清楚特立帕肽对骨膜蛋白的作用。
确定特立帕肽治疗对循环骨形成调节因子骨膜蛋白水平的影响，并研究骨膜蛋白变化与骨转换标志物、骨形成调节因子和骨密度（BMD）变化的关系。
20 名骨质疏松症女性；为期 2 年的开放标签单臂研究。
特立帕肽 20µg，每日皮下注射，共 104 周。基线（两次就诊）和第 1、2、4、12、26、52、78 和 104 周时采集空腹血清，测量骨膜蛋白、硬化素和 Dickkopf 相关蛋白 1、I 型前胶原氨基端前肽（PINP）和 I 型胶原 C 端肽。使用双能 X 射线吸收法测量腰椎、全髋和股骨颈的 BMD。
特立帕肽治疗 26 周后，骨膜蛋白水平升高 6.6%（95%可信区间，-0.4 至 13.5），52 周后显著升高 12.5%（95%可信区间，3.3 至 21.0；P<0.01）。骨膜蛋白的变化与第 52 周腰椎 BMD 的变化呈正相关（r=0.567；95%可信区间，0.137 至 0.817；P<0.05），与第 104 周股骨颈 BMD 的变化呈正相关（r=0.682；95%可信区间，0.261 至 0.885；P<0.01）。
特立帕肽治疗可增加骨膜蛋白分泌；尚不清楚这种增加是否介导了药物对骨骼的作用。
