Biotechnology Research Center, Mashhad University of Medical Sciences, Mashhad, 9177948564, Iran; Metabolic Research Centre, Royal Perth Hospital, School of Medicine and Pharmacology, University of Western Australia, Perth, Australia.
University Hospital Center Zagreb, Department of Internal medicine, Kišpatićeva 12, Zagreb, Croatia.
Metabolism. 2016 Nov;65(11):1664-1678. doi: 10.1016/j.metabol.2016.08.007. Epub 2016 Aug 31.
Lipoprotein(a) (Lp(a)) is a proatherogenic and prothrombotic lipoprotein. Our aim was to quantify the extended-release nicotinic acid Lp(a) reducing effect with a meta-analysis of the available randomized clinical trials.
A meta-analysis and random-effects meta-regression were performed on data pooled from 14 randomized placebo-controlled clinical trials published between 1998 and 2015, comprising 17 treatment arms, which included 9013 subjects, with 5362 in the niacin arm.
The impact of ER niacin on plasma Lp(a) concentrations was reported in 17 treatment arms. Meta-analysis suggested a significant reduction of Lp(a) levels following ER niacin treatment (weighted mean difference - WMD: -22.90%, 95% CI: -27.32, -18.48, p<0.001). Results also remained similar when the meta-analysis was repeated with standardized mean difference as summary statistic (WMD: -0.66, 95% CI: -0.82, -0.50, p<0.001). When the studies were categorized according to the administered dose, there was a comparable effect between the subsets of studies with administered doses of <2000mg/day (WMD: -21.85%, 95% CI: -30.61, -13.10, p<0.001) and ≥2000mg/day (WMD: -23.21%, 95% CI: -28.41, -18.01, p<0.001). The results of the random-effects meta-regression did not suggest any significant association between the changes in plasma concentrations of Lp(a) with dose (slope: -0.0001; 95% CI: -0.01, 0.01; p=0.983), treatment duration (slope: -0.40; 95% CI: -0.97, 0.17; p=0.166), and percentage change in plasma HDL-C concentrations (slope: 0.44; 95% CI: -0.48, 1.36; p=0.350).
In this meta-analysis of randomized placebo-controlled clinical trials, treatment with nicotinic acid was associated with a significant reduction in Lp(a) levels.
脂蛋白（a）（Lp(a)）是一种促动脉粥样硬化和促血栓形成的脂蛋白。我们的目的是通过对现有随机临床试验的荟萃分析来量化烟酸的持续释放对 Lp(a)的降低作用。
对 1998 年至 2015 年期间发表的 14 项随机安慰剂对照临床试验的数据进行了荟萃分析和随机效应荟萃回归，共包括 17 个治疗组，其中包括 9013 名受试者，烟酸组 5362 名。
17 个治疗组报告了 ER 烟酸对血浆 Lp(a)浓度的影响。荟萃分析表明，烟酸治疗后 Lp(a)水平显著降低（加权平均差异-WMD：-22.90%，95%CI：-27.32，-18.48，p<0.001）。当使用标准化均数差作为汇总统计量时，荟萃分析结果仍然相似（WMD：-0.66，95%CI：-0.82，-0.50，p<0.001）。当根据给药剂量对研究进行分类时，<2000mg/天（WMD：-21.85%，95%CI：-30.61，-13.10，p<0.001）和≥2000mg/天（WMD：-23.21%，95%CI：-28.41，-18.01，p<0.001）亚组之间的效果相当。随机效应荟萃回归的结果表明，Lp(a) 血浆浓度的变化与剂量（斜率：-0.0001；95%CI：-0.01，0.01；p=0.983）、治疗持续时间（斜率：-0.40；95%CI：-0.97，0.17；p=0.166）和血浆高密度脂蛋白胆固醇浓度的百分比变化（斜率：0.44；95%CI：-0.48，1.36；p=0.350）之间没有显著关联。
在这项随机安慰剂对照临床试验的荟萃分析中，烟酸治疗与 Lp(a)水平的显著降低相关。
