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首页> 美国卫生研究院文献>The Journal of Neurology and Psychopathology >Amelioration of osteopenia and hypovitaminosis D by1α-hydroxyvitamin D3 in elderly patients with Parkinsons disease
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Amelioration of osteopenia and hypovitaminosis D by1α-hydroxyvitamin D3 in elderly patients with Parkinsons disease

机译：骨质疏松症和维生素D缺乏症的改善帕金森氏病老年患者中的1α-羟基维生素D3

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OBJECTIVES—A high prevalence of hip and other fractures in elderly patients with Parkinson's disease has been linked to reduced bone mass arising from a defect of renal synthesis of 1, 25-dihydroxyvitamin D (1, 25-[OH]2D). Treatment with 1α-hydroxyvitamin D3 (1α(OH)D3; an active form of vitamin D) was evaluated for maintaining bone mass and reducing the incidence of hip and other non-vertebral fractures in patients with Parkinson's disease.
METHODS—In a double blind, randomised trial, 86 elderly patients with Parkinson's disease (mean Hoehn and Yahr stage, 3; mean age 70.6 years) were randomised to receive either 1 µg 1α(OH)D3 daily (treatment group, n=43) or a placebo (n=43) for 18 months. Bone mineral densities in the second metacarpals were determined by computed radiographic densitometry. Serum bone turnover indices were measured serially, and incidence of non-vertebral fractures was recorded.
RESULTS—Bone mineral densities decreased 1.2% in the treatment group compared with 6.7% in the placebo group during 18 months (p<0.0001). At baseline in both groups, the serum concentration of 1, 25-[OH]2D was reduced. Parathyroid hormone was abnormally increased in 15patients(17%) and correlated negatively with serum 25-hydroxyvitamin D,indicating compensatory hyperparathyroidism. Eight patients sustainedfractures (six at the hip and two at other sites) in the placebo group,and one hip fracture occurred among treated patients (odds ratio 9.8;p=0.0028).
CONCLUSION—Byincreasing serum 1, 25-[OH]2D concentrations, treatmentwith 1α(OH)D3 can reduce the risk of hip and other non-vertebral fractures in osteoporotic elderly patients with Parkinson's disease byslowing the loss of bone mineral densities.
机译：目的—帕金森氏病老年患者的髋部和其他骨折患病率较高，与肾合成1，25-二羟基维生素D（1，25- [OH] 2D）缺陷引起的骨量减少有关。评估了1α-羟基维生素D3（1α（OH）D3；维生素D的一种活性形式）的治疗，以维持骨量并减少帕金森氏病患者的髋部和其他非椎骨骨折的发生率。
方法-在一项双盲，随机试验中，将86例帕金森氏病老年患者（平均Hoehn和Yahr期，3岁；平均年龄70.6岁）随机接受每日1 µg1α（OH）D3治疗（治疗组，n = 43）或安慰剂（n = 43），持续18个月。第二掌骨中的骨矿物质密度通过计算机射线照相光密度法测定。连续测量血清骨转换指数，并记录非椎骨骨折的发生率。
结果—在18个月内，治疗组的骨矿物质密度降低了1.2％，而安慰剂组的骨矿物质密度降低了6.7％（p <0.0001） 。两组在基线时，血清1，25- [OH] 2D的浓度均降低。 15名患者的甲状旁腺激素异常增加（17％）与血清25-羟基维生素D呈负相关，说明代偿性甲状旁腺功能亢进。持续八名患者安慰剂组骨折（髋部骨折六处，其他部位骨折两处），接受治疗的患者中有1例发生髋部骨折（比值9.8；p = 0.0028）。
结论—通过增加血清1、25- [OH] 2D的浓度，治疗1α（OH）D3可以通过以下方法降低骨质疏松老年帕金森病患者的髋部和其他非椎骨骨折风险减缓骨骼矿物质密度的损失。

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