维生素D和炎症。

Dermato-Endocrinology Pub Date : 2015-01-29 eCollection Date: 2014-01-01 DOI:10.4161/19381980.2014.983401
John J Cannell, William B Grant, Michael F Holick
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引用次数: 351

摘要

一些研究发现25-羟基维生素D [25(OH)D]与炎症标志物之间呈反比关系。关于维生素D是否降低炎症或炎症是否降低25(OH)D浓度存在争议。大手术后25(OH)D浓度肯定会下降。然而,这是由于炎症降低了25(OH)D,还是25(OH)D被身体代谢清除以平息炎症。我们检索了文献,发现了39项维生素D和炎症标志物的随机对照试验(RCT)。17例发现炎症标志物明显减少,19例没有,1例混合,1例出现不良结果。除了少数例外,对正常受试者、肥胖、2型糖尿病患者和稳定型心血管疾病的研究均未发现显著的有益效果。然而,我们发现维生素D3在高度炎症性疾病(急性婴儿充血性心力衰竭、多发性硬化症、炎症性肠病、囊性纤维化、SLE、活动性结核病和进展性心肌梗死)中的7项随机对照试验中有6项发现显著降低。我们发现基线和最终25(OH)D预测炎症标志物显著降低的rct。当基线25(OH)D水平较低时,当达到25(OH)D水平时,维生素D倾向于适度降低高度炎症条件下的炎症标志物。未来的调查应该:招募基线25(OH)D水平较低的受试者,炎症标志物升高的受试者,有炎症状况的受试者,达到适当的最终25(OH)D水平,并使用生理剂量的维生素D。我们试图确定所有现有的维生素D随机对照试验(rct),这些试验使用炎症标志物作为主要或次要终点。
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Vitamin D and inflammation.

Several studies found an inverse relationship between 25-hydroxyvitamin D [25(OH)D] and markers of inflammation. A controversy exists as to whether vitamin D lowers inflammation or whether inflammation lowers 25(OH)D concentrations. Certainly 25(OH)D concentrations fall after major surgery. However, is this due to inflammation lowering 25(OH)D or is 25(OH)D being metabolically cleared by the body to quell inflammation. We searched the literature and found 39 randomized controlled trials (RCT) of vitamin D and markers of inflammation. Seventeen found significantly reduced inflammatory markers, 19 did not, one was mixed and one showed adverse results. With few exceptions, studies in normal subjects, obesity, type 2 diabetics, and stable cardiovascular disease did not find significant beneficial effects. However, we found that 6 out of 7 RCTS of vitamin D3 in highly inflammatory conditions (acute infantile congestive heart failure, multiple sclerosis, inflammatory bowel disease, cystic fibrosis, SLE, active TB and evolving myocardial infarction) found significant reductions. We found baseline and final 25(OH)D predicted RCTs with significant reduction in inflammatory markers. Vitamin D tends to modestly lower markers of inflammation in highly inflammatory conditions, when baseline 25(OH)D levels were low and when achieved 25(OH)D levels were higher. Future inquiries should: recruit subjects with low baseline 25(OH)D levels, subjects with elevated markers of inflammation, subjects with inflammatory conditions, achieve adequate final 25(OH)D levels, and use physiological doses of vitamin D. We attempted to identify all extant randomized controlled trials (RCTs) of vitamin D that used inflammatory markers as primary or secondary endpoints.

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