Omega-3 Fatty Acid Supplementation Improves Endothelial Function in Primary Antiphospholipid Syndrome: A Small-Scale Randomized Double-Blind Placebo-Controlled Trial

Omega-3 Fatty Acid Supplementation Improves Endothelial Function in Primary Antiphospholipid Syndrome: A Small-Scale Randomized Double-Blind Placebo-Controlled Trial
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DOI:
10.3389/fimmu.2018.00336
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发表时间:
2018-03-02
影响因子:
7.3
通讯作者:
Benatti, Fabiana B.
Benatti, Fabiana B.
中科院分区:
医学2区
文献类型:
--
作者:
Felau, Sheylla M.;Sales, Lucas P.;Benatti, Fabiana B.

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被引文献

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内皮细胞被认为在抗磷脂综合征(APS)的发病机制中发挥着核心作用。补充 Omega-3 多不饱和脂肪酸 (n-3 PUFA) 已被证明可以改善多种疾病的内皮功能;因此,它在 APS 中可能具有高度的临床相关性。本研究的目的是评估补充 n-3 PUFA 对原发性 APS (PAPS) 患者内皮功能(主要结果)的功效。对 22 名患有 PAPS 的成年女性进行了一项为期 16 周的随机临床试验。患者被随机分配 (1:1) 接受安慰剂 (PL, n = 11) 或 n-3 PUFA (omega-3, n = 11) 补充剂。干预前(前)和后(后)16 周,对患者的内皮功能(外周动脉张力测定)进行评估(主要结果)。还评估了患者的内皮细胞活化的全身标志物、炎症标志物、饮食摄入量、国际标准化比率(INR)和不良反应。与 PL 相比,omega-3 组术后内皮功能估计反应性充血指数 (RHI) 和 RHI 对数变换 (LnRHI) 显着增加(+13 vs. -12%,rho = 0.06,ES = 0.9;+23 vs. -22%,rho = 0.02,ES = 1.0)。未观察到 e-选择素、血管粘附分子-1 和纤维蛋白原水平发生变化 (rho > 0.05)。此外,omega-3组显示白细胞介素10(-4 vs. +45%,rho = 0.04,ES = -0.9)和肿瘤坏死因子(-13 vs. +0.3%,rho = 0.04,ES = -0.95)的循环水平降低,并且细胞间粘附分子-1反应有较低的趋势(+3 vs. +48%,rho = 0.1,ES = -0.7) 与 PL 相比,后期。未观察到饮食摄入量、INR 或自我报告的不良反应发生变化。总之,16 周的 n-3 PUFA 补充剂改善了控制良好的 PAPS 患者的内皮功能。这些结果支持补充 n-3 PUFA 作为 APS 辅助治疗的作用。在 http://ClinicalTrials.gov 注册为 NCT01956188。
Endothelial cells are thought to play a central role in the pathogenesis of antiphospholipid syndrome (APS). Omega-3 polyunsaturated fatty acid (n-3 PUFA) supplementation has been shown to improve endothelial function in a number of diseases; thus, it could be of high clinical relevance in APS. The aim of this study was to evaluate the efficacy of n-3 PUFA supplementation on endothelial function (primary outcome) of patients with primary APS (PAPS). A 16-week randomized clinical trial was conducted with 22 adult women with PAPS. Patients were randomly assigned (1:1) to receive placebo (PL, n = 11) or n-3 PUFA (omega-3, n = 11) supplementation. Before (pre) and after (post) 16 weeks of the intervention, patients were assessed for endothelial function (peripheral artery tonometry) (primary outcome). Patients were also assessed for systemic markers of endothelial cell activation, inflammatory markers, dietary intake, international normalized ratio (INR), and adverse effects. At post, omega-3 group presented significant increases in endothelial function estimates reactive hyperemia index (RHI) and logarithmic transformation of RHI (LnRHI) when compared with PL (+13 vs. -12%, rho = 0.06, ES = 0.9; and +23 vs. -22%, rho = 0.02, ES = 1.0). No changes were observed for e-selectin, vascular adhesion molecule-1, and fibrinogen levels (rho > 0.05). In addition, omega-3 group showed decreased circulating levels of interleukin-10 (-4 vs. +45%, rho = 0.04, ES = -0.9) and tumor necrosis factor (-13 vs. +0.3%, rho = 0.04, ES = -0.95) and a tendency toward a lower intercellular adhesion molecule-1 response (+3 vs. +48%, rho = 0.1, ES = -0.7) at post when compared with PL. No changes in dietary intake, INR, or self-reported adverse effects were observed. In conclusion, 16 weeks of n-3 PUFA supplementation improved endothelial function in patients with well-controlled PAPS. These results support a role of n-3 PUFA supplementation as an adjuvant therapy in APS. Registered at http://ClinicalTrials.gov as NCT01956188.