Viljakainen Heli T, Natri Anna-Mari, Kärkkäinen Merja, Huttunen Minna M, Palssa Anette, Jakobsen Jette, Cashman Kevin D, Mølgaard Christian, Lamberg-Allardt Christel
Calcium Research Unit, Department of Applied Chemistry and Microbiology, University of Helsinki, Helsinki, Finland.
J Bone Miner Res. 2006 Jun;21(6):836-44. doi: 10.1359/jbmr.060302.
The effect of vitamin D supplementation on bone mineral augmentation in 212 adolescent girls with adequate calcium intake was studied in a randomized placebo-controlled setting. Bone mineral augmentation determined by DXA increased with supplementation both in the femur and the lumbar vertebrae in a dose-responsive manner. Supplementation decreased the urinary excretion of resorption markers, but had no impact on formation markers.
Adequate vitamin D intake protects the elderly against osteoporosis, but there exists no indisputable evidence that vitamin D supplementation would benefit bone mineral augmentation. The aim of this 1-year study was to determine in a randomized double-blinded trial the effect of 5 and 10 microg vitamin D3 supplementation on bone mineral augmentation in adolescent girls with adequate dietary calcium intake.
Altogether, 228 girls (mean age, 11.4 +/- 0.4 years) participated. Their BMC was measured by DXA from the femur and lumbar spine. Serum 25-hydroxyvitamin D [S-25(OH)D], intact PTH (S-iPTH), osteocalcin (S-OC), and urinary pyridinoline (U-Pyr) and deoxypyridinoline (U-Dpyr) were measured. Statistical analysis was performed both with the intention-to-treat (IT) and compliance-based (CB) method.
In the CB analysis, vitamin D supplementation increased femoral BMC augmentation by 14.3% with 5 microg and by 17.2% with 10 microg compared with the placebo group (ANCOVA, p = 0.012). A dose-response effect was observed in the vertebrae (ANCOVA, p = 0.039), although only with the highest dose. The mean concentration of S-25(OH)D increased (p < 0.001) in the 5-microg group by 5.7 +/- 15.7 nM and in the 10-microg group by 12.4 +/- 13.7 nM, whereas it decreased by 6.7 +/- 11.3 nM in the placebo group. Supplementation had no effect on S-iPTH or S-OC, but it decreased U-DPyr (p = 0.042).
Bone mineral augmentation in the femur was 14.3% and 17.2% higher in the groups receiving 5 and 10 microg of vitamin D, respectively, compared with the placebo group, but only 10 mug increased lumbar spine BMC augmentation significantly. Vitamin D supplementation decreased the concentration of bone resorption markers, but had no impact on bone formation markers, thus explaining increased bone mineral augmentation. However, the positive effects were noted with the CB method but not with IT.
在一项随机安慰剂对照试验中,研究了补充维生素D对212名钙摄入量充足的青春期女孩骨矿物质增加的影响。通过双能X线吸收法(DXA)测定,补充维生素D后,股骨和腰椎的骨矿物质增加呈剂量依赖性。补充维生素D可降低骨吸收标志物的尿排泄,但对骨形成标志物无影响。
充足的维生素D摄入可保护老年人预防骨质疏松,但尚无确凿证据表明补充维生素D对骨矿物质增加有益。这项为期1年的研究旨在通过随机双盲试验确定补充5微克和10微克维生素D3对饮食钙摄入量充足的青春期女孩骨矿物质增加的影响。
共有228名女孩(平均年龄11.4±0.4岁)参与。通过DXA测量她们股骨和腰椎的骨密度(BMC)。检测血清25-羟维生素D [S-25(OH)D]、完整甲状旁腺激素(S-iPTH)、骨钙素(S-OC)以及尿吡啶啉(U-Pyr)和脱氧吡啶啉(U-Dpyr)。采用意向性分析(IT)和基于依从性分析(CB)两种方法进行统计分析。
在基于依从性分析中,与安慰剂组相比,补充5微克维生素D组的股骨BMC增加了14.3%,补充10微克维生素D组增加了17.2%(协方差分析,p = 0.012)。在腰椎也观察到剂量反应效应(协方差分析,p = 0.039),尽管仅在最高剂量时出现。5微克组的S-25(OH)D平均浓度增加了5.7±15.7纳摩尔,10微克组增加了12.4±13.7纳摩尔,而安慰剂组降低了6.7±11.3纳摩尔。补充维生素D对S-iPTH或S-OC无影响,但降低了U-DPyr(p = 0.042)。
与安慰剂组相比,分别接受5微克和10微克维生素D的组中,股骨的骨矿物质增加分别高出14.3%和17.2%,但只有10微克组显著增加了腰椎BMC。补充维生素D降低了骨吸收标志物的浓度,但对骨形成标志物无影响,从而解释了骨矿物质增加的原因。然而,积极效果是通过基于依从性分析方法观察到的,而在意向性分析中未观察到。