Power J, Taggart J, Parker M, Berry J L, Reeve J
Department of Biological Sciences, University of Chester, Chester, UK.
Cell Biochem Funct. 2014 Jun;32(4):341-3. doi: 10.1002/cbf.3021. Epub 2013 Dec 27.
There is little information on tissue as distinct from plasma levels of vitamin D metabolites in cases of hip fracture compared with controls. Femoral neck fractures in the elderly are associated with increased cortical remodelling and endosteal resorption, leading to regional increases in porosity and reduced cortical thickness. Vitamin D metabolites play a central role in the maintenance of normal serum calcium levels and may, through interactions with parathyroid hormone, exert an important influence on bone structure. To investigate whether hip fracture might be associated with tissue vitamin D deficiency, we have measured by radioimmunoassay the levels of 25 hydroxy vitamin D (25 (OH)D) in bone marrow samples extracted from the proximal femurs of 16 female subjects who had suffered fracture (mean age = 82.1 years, standard error (se) 1.9) and nine sex matched post mortem controls (mean age = 83.8 years, se 2.5). Twenty five (OH)D concentrations were significantly greater in the fracture cases (median = 3.7, IQR = 2.5-3.9 ng/g) than in the control group (median = 1.5, IQR = 0.9-2.3 ng/g; P = 0.0007, non-parametric Wilcoxon/Kruskal-Wallis test). It was suggested in the 1970s that bone loss and hip fracture risk in the UK were driven by vitamin D deficiency. Our results suggest that the alterations in femoral neck bone microstructure and remodelling in hip fracture cannot be assigned to the single cause of relative deficiency of vitamin D. Vitamin D deficiency or insufficiency may nevertheless increase remodelling and loss of bone tissue and contribute causally to a minority of hip fractures.
与对照组相比，关于髋部骨折患者维生素D代谢物的组织水平（与血浆水平不同）的信息很少。老年人的股骨颈骨折与皮质重塑增加和骨内膜吸收有关，导致局部孔隙率增加和皮质厚度减小。维生素D代谢物在维持正常血清钙水平中起核心作用，并可能通过与甲状旁腺激素的相互作用，对骨骼结构产生重要影响。为了研究髋部骨折是否可能与组织维生素D缺乏有关，我们通过放射免疫分析法测量了从16名骨折女性受试者（平均年龄 = 82.1岁，标准误差（se）1.9）和9名性别匹配的死后对照组（平均年龄 = 83.8岁，se 2.5）的股骨近端提取的骨髓样本中25羟基维生素D（25（OH）D）的水平。骨折病例中的25（OH）D浓度（中位数 = 3.7，四分位间距 = 2.5 - 3.9 ng/g）显著高于对照组（中位数 = 1.5，四分位间距 = 0.9 - 2.3 ng/g；P = 0.0007，非参数Wilcoxon/Kruskal-Wallis检验）。在20世纪70年代有人提出，英国的骨质流失和髋部骨折风险是由维生素D缺乏驱动的。我们的结果表明，髋部骨折时股骨颈骨微结构和重塑的改变不能归因于维生素D相对缺乏这一单一原因。然而，维生素D缺乏或不足可能会增加骨组织的重塑和流失，并在少数髋部骨折中起因果作用。
