Department of Orthopaedic Surgery, Hospital for Special Surgery, 535 East 70th Street, New York, NY 10021, USA.
Clin Orthop Relat Res. 2012 Mar;470(3):927-36. doi: 10.1007/s11999-011-2029-1. Epub 2011 Aug 24.
Fracture leads to local and systemic catabolic physiologic changes. As teriparatide is an agent used to treat osteoporosis in patients with fragility fractures, it is unclear whether teriparatide treatment alters bone mineral density (BMD) and bone markers when given to patients with fractures.
QUESTIONS/PURPOSES: We asked whether BMD and bone marker responses would be blunted in patients with fractures placed on teriparatide after fracture compared with patients without fractures on teriparatide.
We retrospectively collected data from 141 patients treated with teriparatide for osteoporosis. Seventy-seven patients received teriparatide after fractures (fracture group), whereas 64 were treated for other indications (nonfracture group). We determined BMD at the lumbar spine and at the proximal femur before and 12 and 24 months posttreatment. Bone markers (urine N-telopeptide [urine NTX], bone-specific alkaline phosphatase [BALP]) were measured at baseline and 3, 12, and 24 months posttreatment.
Mean lumbar spine and hip BMDs at last followup increased from baseline with no differences between groups to approximately 9% and 4% at 24 months, respectively. Both bone markers increased from baseline in the nonfracture group, peaking at 12 months. For the fracture group, only urine NTX increased at 3 and 12 months posttreatment. Although the peak levels of both bone markers in the nonfracture group were greater, there was no difference between the two groups.
Fracture does not have a negative effect on the BMD and bone marker responses to teriparatide treatment. Clinicians should anticipate comparable BMD responses when treating patients with teriparatide for osteoporotic fractures and for other indications.
Level III, therapeutic study. See Guidelines for Authors for a complete description of levels of evidence.
骨折会导致局部和全身分解代谢的生理变化。特立帕肽是一种用于治疗脆性骨折患者骨质疏松症的药物，目前尚不清楚在骨折患者中使用特立帕肽治疗是否会改变骨密度（BMD）和骨标志物。
问题/目的：我们想知道与没有骨折的特立帕肽治疗患者相比，骨折后接受特立帕肽治疗的患者的 BMD 和骨标志物反应是否会减弱。
我们回顾性收集了 141 例接受特立帕肽治疗骨质疏松症的患者数据。77 例患者在骨折后接受特立帕肽治疗（骨折组），64 例患者因其他适应证接受特立帕肽治疗（非骨折组）。我们在治疗前和治疗后 12 个月和 24 个月时分别测定腰椎和股骨近端的 BMD。在治疗前和治疗后 3、12 和 24 个月时测定骨标志物（尿 N-端肽[尿 NTX]、骨碱性磷酸酶[BALP]）。
末次随访时，腰椎和髋部 BMD 均值较基线水平分别增加了 9%和 4%，两组间无差异。两组的骨标志物均在非骨折组中从基线水平升高，在 12 个月时达到峰值。对于骨折组，仅在治疗后 3 个月和 12 个月时尿 NTX 增加。尽管非骨折组的两种骨标志物的峰值水平较高，但两组间无差异。
骨折不会对特立帕肽治疗的 BMD 和骨标志物反应产生负面影响。当使用特立帕肽治疗骨质疏松性骨折和其他适应证的患者时，临床医生应预期会有类似的 BMD 反应。
三级，治疗性研究。欲了解完整的证据水平描述，请参见作者指南。
