School of Health Science, La Trobe University, Bundoora, Australia.
The Florey Institute of Neuroscience and Mental Health, University of Melbourne, Heidelberg, Australia.
Arch Osteoporos. 2018 Jan 8;13(1):5. doi: 10.1007/s11657-017-0414-4.
Bone fragility contributes to increased fracture risk, but little is known about the emergence of post-stroke bone loss. We investigated skeletal changes and relationships with physical activity, stroke severity, motor control and lean mass within 6 months of stroke.
This is a prospective observational study. Participants were non-diabetic but unable to walk within 2 weeks of first stroke. Distal tibial volumetric bone mineral density (vBMD, primary outcome), bone geometry and microstructure (high-resolution peripheral quantitative computed tomography) were assessed at baseline and 6 months, as were secondary outcomes total body bone mineral content and lean mass (dual energy X-ray absorptiometry), bone metabolism (serum osteocalcin, N-terminal propeptide of type 1 procollagen (P1NP), C-terminal telopeptide of type 1 collagen (CTX)), physical activity (PAL2 accelerometer) and motor control (Chedoke McMaster) which were also measured at 1 and 3 months.
Thirty-seven participants (69.7 years (SD 11.6), 37.8% females, NIHSS 12.6 (SD 4.7)) were included. The magnitude of difference in vBMD between paretic and non-paretic legs increased within 6 months, with a greater reduction observed in paretic legs (mean difference = 1.5% (95% CI 0.5, 2.6), p = 0.007). At 6 months, better motor control was associated with less bone loss since stroke (r = 0.46, p = 0.02). A trend towards less bone loss was observed in people who regained independent walking compared to those who did not (p = 0.053). Higher baseline daily count of standing up was associated with less change in bone turnover over 6 months: osteocalcin (r = -0.51, p = 0.01), P1NP (r = -0.47, p = 0.01), CTX (r = -0.53, p = 0.01).
Better motor control and walking recovery were associated with reduced bone loss. Interventions targeting these impairments from early post-stroke are warranted.
URL: http://www.anzctr.org.au . Unique identifier: ACTRN12612000123842.
骨脆性会导致骨折风险增加,但人们对中风后骨丢失的发生知之甚少。我们研究了中风后 6 个月内骨骼变化与体力活动、中风严重程度、运动控制和瘦体重之间的关系。
这是一项前瞻性观察性研究。参与者为非糖尿病患者,但在首次中风后 2 周内无法行走。基线和 6 个月时评估了远端胫骨体积骨矿物质密度(主要结局)、骨几何形状和微观结构(高分辨率外周定量计算机断层扫描),还评估了全身骨矿物质含量和瘦体重(双能 X 射线吸收法)、骨代谢(血清骨钙素、I 型前胶原 N 端前肽(P1NP)、I 型胶原 C 端肽(CTX))、体力活动(PAL2 加速度计)和运动控制(Chedoke McMaster),这些指标也在 1 个月和 3 个月时进行了测量。
37 名参与者(69.7 岁(标准差 11.6),37.8%女性,NIHSS 12.6(标准差 4.7))被纳入。在 6 个月内,患侧和非患侧腿之间的 vBMD 差异幅度增加,患侧腿的骨丢失更为明显(平均差异为 1.5%(95%CI 0.5, 2.6),p=0.007)。6 个月时,运动控制越好,与中风后骨丢失越少相关(r=0.46,p=0.02)。与未恢复独立行走的人相比,恢复独立行走的人骨丢失减少(p=0.053)。与 6 个月内骨转换变化相比,较高的基线每日站立次数与骨钙素(r=-0.51,p=0.01)、P1NP(r=-0.47,p=0.01)和 CTX(r=-0.53,p=0.01)的变化减少相关。
运动控制更好和行走恢复与骨丢失减少相关。需要针对中风后早期的这些损伤进行干预。