Neuroendocrine Unit (P.K.F., I.S.W., K.K.M., M.M., A.K.), Biostatistics Center (H.L.), and Endocrine Unit (J.S.F.), Massachusetts General Hospital, Boston, Massachusetts 02114; Center for Advanced Orthopaedic Studies (M.L.B.), Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215; and Harvard Medical School (P.K.F., K.K.M., D.B.H., M.M., H.L., J.S.F., M.L.B., A.K.), Boston, Massachusetts 02115.
J Clin Endocrinol Metab. 2014 Apr;99(4):1322-9. doi: 10.1210/jc.2013-4105. Epub 2014 Jan 23.
Anorexia nervosa (AN), a prevalent psychiatric disorder predominantly affecting women, is characterized by self-induced starvation and low body weight. Increased clinical fractures are common, and most women have low bone mineral density (BMD). Previously investigated treatments have led to no or modest increases in BMD in AN.
Our objective was to investigate the effect of teriparatide (TPT; human PTH[1-34]), an anabolic agent, on low bone mass in women with AN.
DESIGN, SETTING, AND PATIENTS: This randomized, placebo-controlled trial at a clinical research center included 21 women with AN: 10 (mean age ± SEM, 47 ± 2.7 years) treated with TPT and 11 (47.1 ± 2.3 years) treated with placebo.
TPT (20 μg s.c.) or placebo was administered for 6 months.
Our primary outcome measure was change in BMD of the spine and hip by dual-energy x-ray absorptiometry. Secondary outcome measures included changes in serum N-terminal propeptide of type 1 procollagen (P1NP), C-terminal collagen cross-links, sclerostin, and IGF-1 levels.
At 6 months, spine BMD increased significantly more with TPT (posteroanterior spine, 6.0% ± 1.4%; lateral spine, 10.5% ± 2.5%) compared with placebo (posteroanterior spine, 0.2% ± 0.7%, P < .01; lateral spine, -0.6% ± 1.0%; P < .01). The results remained significant after controlling for baseline body mass index, P1NP, and IGF-1. Changes in femoral neck (P = .4) and total hip (P = 0.8) BMD were comparable in both groups, as were changes in weight. Serum P1NP levels increased after 3 months of TPT treatment and remained at this higher level at 6 months, whereas P1NP levels were unchanged in the placebo group (P = .02). TPT was well-tolerated by all subjects.
This study demonstrates that TPT administration increases spine BMD substantially after only 6 months of therapy in women with AN.
神经性厌食症(AN)是一种常见的精神疾病,主要影响女性,其特征是自我诱导的饥饿和低体重。临床骨折的发生率较高,大多数女性的骨密度(BMD)较低。先前研究的治疗方法并未导致 AN 患者的 BMD 有显著增加。
我们旨在研究促甲状旁腺激素(TPT;人 PTH[1-34]),一种合成代谢药物,对 AN 患者低骨量的影响。
设计、地点和患者:这项在临床研究中心进行的随机、安慰剂对照试验纳入了 21 名 AN 女性患者:10 名(平均年龄 ± SEM,47 ± 2.7 岁)接受 TPT 治疗,11 名(47.1 ± 2.3 岁)接受安慰剂治疗。
TPT(20μg 皮下注射)或安慰剂治疗 6 个月。
我们的主要观察指标是双能 X 射线吸收仪测量的脊柱和髋部骨密度变化。次要观察指标包括血清 1 型前胶原 N 端前肽(P1NP)、C 端胶原交联、骨硬化蛋白和 IGF-1 水平的变化。
6 个月时,TPT 治疗组的脊柱 BMD 显著增加(前后位脊柱增加 6.0%±1.4%;侧位脊柱增加 10.5%±2.5%),而安慰剂组仅增加 0.2%±0.7%(前后位脊柱,P<.01;侧位脊柱,P<.01)。控制基线体重指数、P1NP 和 IGF-1 后,结果仍有统计学意义。两组的股骨颈(P=0.4)和全髋(P=0.8)BMD 变化相似,体重变化也相似。TPT 治疗 3 个月后血清 P1NP 水平升高,并持续升高至 6 个月,而安慰剂组 P1NP 水平无变化(P=0.02)。所有患者均能耐受 TPT。
这项研究表明,在 AN 女性中,TPT 治疗仅 6 个月后,脊柱 BMD 就显著增加。