Szollar S M, Martin E M, Sartoris D J, Parthemore J G, Deftos L J
Department of Orthopedic Rehabilitation, University of California, San Diego, USA.
Am J Phys Med Rehabil. 1998 Jan-Feb;77(1):28-35. doi: 10.1097/00002060-199801000-00005.
We evaluated the pattern of osteoporosis after spinal cord injury, determined the time-frame of the changes, and elucidated the relationship among parathyroid hormone levels, biochemical markers of bone formation, and the pattern of bone mass loss. We included 176 subjects with spinal cord injury and 62 subjects without spinal cord injury as controls in the study. Bone mineral density of the spine and the proximal femur was measured. The participants' age, level of injury, and length of time since injury were compared with the nonspinal cord-injured controls and with each other. Serum levels of calcium, calcitonin, biochemical markers of bone formation, and parathyroid hormone were determined. Our results revealed that bone mineral density of the proximal femur declined and reached fracture threshold at one to five years after injury. The decline was detected at 12 months after injury in all age groups. Spinal bone mineral density neither declined significantly nor reached fracture threshold. Parathyroid hormone levels declined before the end of the first year postinjury and increased at one to nine years postinjury in the 20- to 39-year age group. The increase correlated with the initial decline of bone mineral density of the proximal femur. Our studies in spinal cord-injured subjects revealed a pattern of osteoporosis similar to age and parathyroid dysfunction-related osteoporosis. No other correlation was detected between indexes of bone metabolism and bone mineral density measurements.
我们评估了脊髓损伤后骨质疏松的模式,确定了变化的时间框架,并阐明了甲状旁腺激素水平、骨形成生化标志物与骨量丢失模式之间的关系。我们纳入了176例脊髓损伤患者和62例无脊髓损伤的受试者作为对照进行研究。测量了脊柱和股骨近端的骨密度。将参与者的年龄、损伤水平和受伤后的时间长度与无脊髓损伤的对照组以及彼此进行比较。测定了血清钙、降钙素、骨形成生化标志物和甲状旁腺激素的水平。我们的结果显示,股骨近端骨密度在受伤后1至5年下降并达到骨折阈值。所有年龄组在受伤后12个月均检测到骨密度下降。脊柱骨密度既没有显著下降,也没有达到骨折阈值。在20至39岁年龄组中,甲状旁腺激素水平在受伤后第一年末之前下降,并在受伤后1至9年升高。这种升高与股骨近端骨密度的初始下降相关。我们对脊髓损伤患者的研究揭示了一种与年龄和甲状旁腺功能障碍相关的骨质疏松类似的骨质疏松模式。在骨代谢指标与骨密度测量之间未检测到其他相关性。