Effect of Vitamin D Supplementation on Blood Pressure: A Systematic Review and Meta-analysis Incorporating Individual Patient Data.
Effect of Vitamin D Supplementation on Blood Pressure: A Systematic Review and Meta-analysis Incorporating Individual Patient Data.
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DOI：
10.1001/jamainternmed.2015.0237
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发表时间：
2015-05
影响因子：
39
通讯作者：
D-PRESSURE Collaboration
中科院分区：
文献类型：
--
作者：
Beveridge LA;Struthers AD;Khan F;Jorde R;Scragg R;Macdonald HM;Alvarez JA;Boxer RS;Dalbeni A;Gepner AD;Isbel NM;Larsen T;Nagpal J;Petchey WG;Stricker H;Strobel F;Tangpricha V;Toxqui L;Vaquero MP;Wamberg L;Zittermann A;Witham MD;D-PRESSURE Collaboration
维生素 D 水平低与血压 (BP) 升高和未来的心血管事件有关。补充维生素 D 是否会降低血压以及哪些患者特征可预测疗效仍不清楚。系统评价补充维生素 D 或其类似物是否可以降低血压。我们检索了 MEDLINE、CINAHL、EMBASE、Cochrane 对照试验中心注册库和 http://www.ClinicalTrials.com，并手动检索了所包含的文章和之前的评论中的参考文献。在谷歌上搜索灰色文献（即未在公认的科学期刊上发表的材料）。没有应用语言限制。检索期涵盖 1966 年 1 月 1 日至 2014 年 3 月 31 日。我们纳入了随机安慰剂对照临床试验，这些试验针对任何适应症使用维生素 D 补充剂至少 4 周，并报告了血压数据。如果他们使用活性或非活性形式的维生素 D 或维生素 D 类似物，则纳入研究。如果所有治疗组都相同，则允许进行联合干预。我们提取了基线人口统计数据、25-羟基维生素 D 水平、收缩压和舒张压（SBP 和 DBP）以及从基线到最终随访的血压变化数据。纳入研究的作者要求提供有关年龄、性别、药物使用、糖尿病、基线和随访血压以及 25-羟基维生素 D 水平的个体患者数据。对于试验水平数据，血压变化的组间差异被合并到随机效应模型中。对于个体患者数据，在合并到随机效应模型之前计算最终随访时的组间血压差异，并根据基线血压进行调整。在办公室环境中测量的收缩压和舒张压的差异。我们在试验级荟萃分析中纳入了 46 项试验（4541 名受试者）。获得了 27 项试验（3092 名受试者）的个体患者数据。在试验水平上，补充维生素 D 对 SBP（效应值，0.0 [95% CI，-0.8 至 0.8] mm Hg；P = .97；I2 = 21%）或 DBP（效应值，-0.1 [95% CI，-0.6 至 0.5] mm Hg；P = .84；I2 = 20%）没有影响。分析 SBP（效应值，-0.5 [95% CI，-1.3 至 0.4] mm Hg；P = .27；I2 = 0%）和 DBP（效应值，0.2 [95% CI，-0.3 至 0.7] mm Hg；P = .38；I2 = 0%）的个体患者数据时发现了类似的结果。亚组分析没有揭示任何预测治疗反应更好的基线因素。维生素 D 补充剂作为降低血压的药物无效，因此不应用作抗高血压药物。
Low levels of vitamin D are associated with elevated blood pressure (BP) and future cardiovascular events. Whether vitamin D supplementation reduces BP and which patient characteristics predict a response remain unclear. To systematically review whether supplementation with vitamin D or its analogues reduce BP. We searched MEDLINE, CINAHL, EMBASE, Cochrane Central Register of Controlled Trials, and http://www.ClinicalTrials.com augmented by a hand search of references from the included articles and previous reviews. Google was searched for gray literature (ie, material not published in recognized scientific journals). No language restrictions were applied. The search period spanned January 1, 1966, through March 31, 2014. We included randomized placebo-controlled clinical trials that used vitamin D supplementation for a minimum of 4 weeks for any indication and reported BP data. Studies were included if they used active or inactive forms of vitamin D or vitamin D analogues. Cointerventions were permitted if identical in all treatment arms. We extracted data on baseline demographics, 25-hydroxyvitamin D levels, systolic and diastolic BP (SBP and DBP), and change in BP from baseline to the final follow-up. Individual patient data on age, sex, medication use, diabetes mellitus, baseline and follow-up BP, and 25-hydroxyvitamin D levels were requested from the authors of the included studies. For trial-level data, between-group differences in BP change were combined in a random-effects model. For individual patient data, between-group differences in BP at the final follow up, adjusted for baseline BP, were calculated before combining in a random-effects model. Difference in SBP and DBP measured in an office setting. We included 46 trials (4541 participants) in the trial-level meta-analysis. Individual patient data were obtained for 27 trials (3092 participants). At the trial level, no effect of vitamin D supplementation was seen on SBP (effect size, 0.0 [95% CI, −0.8 to 0.8] mm Hg; P = .97; I2 = 21%) or DBP (effect size, −0.1 [95% CI, −0.6 to 0.5] mm Hg; P = .84; I2 = 20%). Similar results were found analyzing individual patient data for SBP (effect size, −0.5 [95% CI, −1.3 to 0.4] mm Hg; P = .27; I2 = 0%) and DBP (effect size, 0.2 [95% CI, −0.3 to 0.7] mm Hg; P = .38; I2 = 0%). Subgroup analysis did not reveal any baseline factor predictive of a better response to therapy. Vitamin D supplementation is ineffective as an agent for lowering BP and thus should not be used as an antihypertensive agent.
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影响因子：
2.3
作者：
Larsen T;Mose FH;Bech JN;Pedersen EB
通讯作者：
Pedersen EB
影响因子：
3.2
作者：
Larsen, Thomas;Mose, Frank H.;Pedersen, Erling B.
通讯作者：
Pedersen, Erling B.
影响因子：
3.7
作者：
Gepner AD;Ramamurthy R;Krueger DC;Korcarz CE;Binkley N;Stein JH
通讯作者：
Stein JH
影响因子：
11.1
作者：
Jorde, R.;Sneve, M.;Figenschau, Y.
通讯作者：
Figenschau, Y.
DOI：
10.1016/j.numecd.2014.02.015
发表时间：
2014-08-01
影响因子：
3.9
作者：
Dalbeni, A.;Scaturro, G.;Delva, P.
通讯作者：
Delva, P.