Lancet Diabetes Endocrinol:老人补充VD预防骨质疏松 这一保健常识将被推翻?

2018-12-23 王淳 环球医学

2018年11月,新西兰和英国学者在《Lancet Diabetes Endocrinol》发表了一项系统评价、Meta分析和试验序贯分析,再次考察了维生素D补充对肌肉骨骼健康的影响。

老年人(>65岁)补充维生素D以治疗或预防骨质疏松,几乎已成为妇孺皆知的保健常识。目前,这一常识面临着被推翻的风险。近期的系统评价报告,补充维生素D对骨密度、跌倒或骨折没有影响。

2018年11月,新西兰和英国学者在《Lancet Diabetes Endocrinol》发表了一项系统评价、Meta分析和试验序贯分析,再次考察了维生素D补充对肌肉骨骼健康的影响。

在这项系统评价、随机效应Meta分析和试验序贯分析中,研究者使用了既往发表的Meta分析中文献检索的结果。通过检索PubMed、Embase和Cochrane Central 2017年9月14日~2018年2月26日发表的文献,研究者对这些结果进行了更新,使用的关键词是“vitamin D”和其他关键词,无语言限制。

研究者评估了成人(>18岁)补充维生素D vs不治疗对照、安慰剂或低剂量维生素D补充的随机对照试验。具有多重干预的试验(如,钙+维生素D)的入组标准为,研究组间仅维生素D使用有差异。研究者排除了羟基化维生素D类似物的试验。符合条件的研究须纳入总体或髋部骨折、跌倒或在腰椎、全髋关节、股骨颈、全身或前臂等部位骨密度等结局的测量数据。

研究者提取了参与者特征、研究设计、干预、结局、资金来源、利益冲突等数据。首要复合终点为至少一次骨折、至少一次髋部骨折或至少一次跌倒的参与者;研究者通过使用所有已有数据的意愿治疗分析,计算骨折和跌倒的相对风险。次要终点为腰椎、全髋关节、股骨颈、全身和前臂骨密度自基线改变的百分比。

研究者筛查出81项随机对照试验(53537人),42项报道了骨折、37项报道了跌倒,41项道了骨密度。

汇总分析中,维生素D对总体骨折(36项试验,44790人,相对风险1.00,95% CI,0.93~1.07)、髋部骨折(20项试验,36655人,相对风险1.11,95% CI,0.97~1.26)、跌倒(37项试验,34144人,相对风险0.97,95% CI,0.93~1.02)无影响。


骨折试验序贯分析


跌倒试验序贯分析

高剂量vs低剂量维生素D的随机对照试验的结果相似,使用高于800IU/d剂量的随机对照试验的亚组分析的结果也相似。

合并分析中,任何部位的骨密度,组间都无临床相关差异(1~5年的范围,-0.16%~0.76%)。

对于总体骨折和跌倒,对于相对风险为15%、10%、7.5%和5%(仅总体骨折),效应估计值位于无效边界内,提示维生素D补充不会降低骨折或跌倒的相对风险。

对于髋部骨折,相对风险为15%,效应估计值介于无效边界和劣效边界间,提示可靠证据表明维生素D补充不会降低髋部骨折15%的相对风险,但其是否增加髋部骨折风险,仍然未知。

对于总体髋部、前臂和全身骨密度,在0.5%的阈值时,效应估计值位于无效边界内,对于腰椎和股骨颈,在1.0%的阈值时,效应估计值位于无效边界内,可靠证据表明维生素D不会改变这些相对风险的结局。

因此,该研究结果表明,补充维生素D无法预防骨折或跌倒,对骨密度也没有具有临床意义的影响。维生素D较高和较低剂量,影响无差异。几乎没有理由认为维生素D补充可维持或改善肌肉骨骼健康。该结论应该反映在临床指南中。

试验序贯分析表明,有可靠的证据表明,补充维生素D没有明显的临床获益:不能使整体骨折的相对风险降低5%,或使跌倒的相对风险降低7.5%,不能使骨密度增加0.5~1%,而且不确定补充维生素D是否潜在增加髋部骨折风险。

进一步开展类似试验也不太可能改变这一试验序贯分析的结论。如果未来某项大型试验的结果与当前试验的结果有显着差异,增加该数据将大幅增加试验结果的异质性,这反过来将减少该项新的大型试验在汇总分析中的权重。因此,总体而言,增加来自大型随机对照试验的阳性结果,对合并结果影响很小,并且不太可能改变meta分析的结论。

原始出处:

Bolland MJ, Grey A and Avenell A. Effects of vitamin D supplementation on musculoskeletal health: a systematic review, meta-analysis, and trial sequential analysis. Lancet Diabetes Endocrinol. 2018 Nov;6(11):847-858. doi: 10.1016/S2213-8587(18)30265-1.

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    2019-03-22 howi
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    2018-12-25 Eleven17

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近日,国际学术期刊 Plos Biology 在线发表了中国科学院生物化学与细胞生物学研究所邹卫国研究组的最新研究成果“H3K36 trimethylation mediated by SETD2 regulates the fate of bone marrow mesenchymal stem cells”,首次揭示了组蛋白甲基转移酶 SETD2 介导的组蛋白 H3k36 三甲基化修饰在骨髓间

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随着年龄增长,最怕骨头出问题导致“动不了”影响生活质量,去医院看病又怕耽误时间。新医改下,分级诊疗政策的逐步落地,这些问题将得到显著缓解。2018年10月20日世界骨质疏松日来临之际,中华医学会骨质疏松和骨矿盐疾病分会在上海发布了《原发性骨质疏松症诊疗社区指导原则》(以下简称社区指导原则),参与编纂的多位权威专家到场并解读社区指导原则的亮点和重要意义,本次新闻发布得到默沙东的支持。 发布仪式

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骨质疏松新的病因和靶点——肠道微生物

骨骼是一个动态活性组织,它通过持续的重塑来维持其矿化平衡及自身的结构完整,其中具有骨形成功能的成骨细胞和具有骨吸收功能的破骨细胞在骨重塑的过程中起着关键的作用。在骨重塑过程中,破骨细胞粘附在旧骨区域,分泌酸性物质溶解矿物质,分泌蛋白酶消化骨基质,形成骨吸收陷窝;然后,成骨细胞移动到被吸收部位,分泌骨基质,骨基质经矿化而形成新骨。正常情况下,破骨与成骨过程有条不紊的进行,它们的平衡是维持正常