哮喘患者中ω-3脂肪酸对支气管高反应性,痰嗜酸粒细胞增多和肥大细胞介质的影响

2014/12/22

   摘要
   背景:
已有报道ω-3脂肪酸补充剂可抑制运动诱发的支气管痉挛(EIB)。但尚未有研究确定ω-3补充剂是否抑制了气道对吸入甘露醇的敏感性,这是一种对轻-中度哮喘患者支气管高反应性(BHR)和EIB模型进行测试的方法。
   方法:在一项双盲、交叉试验中,纳入吸入甘露醇的BHR哮喘患者(N=23,男14例,平均年龄28,其中一半患者规律吸入糖皮质激素),并随机分配到ω-3补充剂(4.0克/天,二十碳五烯酸和2.0克/天,二十二碳六烯酸)组或匹配的对照组,为期3周,随后经过3周的药物洗脱期。主要结果为导致FEV1(PD15)下降15%所需要的甘露醇(毫克)的激发剂量。次要结果为痰嗜酸性粒细胞计数,肺功能检查,哮喘控制问卷(ACQ),血清甘油三脂以及尿液和血清中的脂质介质。
   结果:ω-3脂肪酸(78毫克,51-119)组甘露醇PD15(几何平均数,95%CI)与安慰剂组(88毫克,56-139)(P =0.5)相比无差异。在受试者亚组中(ω-3脂肪酸;8.4±8.2%:安慰剂;7.8±11.8%,P =0.9)(N =11)痰嗜酸性粒细胞无改变(平均值±SD)。在每个治疗期结束时FEV1(%预计值)(ω-3脂肪酸,85±13%:安慰剂组,84±11%,P =0.9)或ACQ(ω-3脂肪酸;1.1±0.5%:安慰剂组1.1±0.5%,P =0.9)(N=23)无显着差异。ω-3脂肪酸可显著降低血中甘油三酯和血清脂肪酸和花生酸代谢物的预期转换,证实了补充的依从性;然而,并没有观察到尿中肥大细胞介质的变化。
   结论:为期3周的ω-3补充剂并不能改善甘露醇引起的BHR,不能降低轻-中度哮喘患者痰嗜酸性粒细胞或抑制尿中肥大细胞介质的排泄,提示膳食中补充ω-3脂肪酸在哮喘短期治疗中并没有多大用处。

 

(苏欣 审校)
Chest. 2014 Oct 16. doi: 10.1378/chest.14-1214. [Epub ahead of print]



 

 

The effect of omega-3 fatty acids on bronchial hyperresponsiveness, sputum eosinophilia and mast cell mediators in asthma.
 

Brannan JD, Bood J, Alkhabaz A, Balgoma D, Otis J, Delin I, Dahlén B, Wheelock CE, Nair P, Dahlén SE, O'Byrne PM.
 

ABSTRACT
BACKGROUND:
Omega-3 fatty acid supplements have been reported to inhibit exercise-induced bronchospasm (EIB). It has not been determined if omega-3 supplements inhibit airway sensitivity to inhaled mannitol, a test for bronchial hyperresponsiveness (BHR) and model for EIB in persons with mild-moderate asthma.
METHODS: In a double-blind, crossover trial, asthmatic subjects who had BHR to inhaled mannitol (n=23, 14 males, mean age 28, half taking regular inhaled corticosteroids) were randomized to omega-3 supplements (4.0g/day eicosapentaenoic acid and 2.0g/day docosahexaenoic acid) or matching placebo for 3-weeks, separated by a 3-week washout. The primary outcome was the provoking dose of mannitol (mg) required to cause a 15% fall in FEV1 (PD15). Secondary outcomes were sputum eosinophil counts, spirometry, asthma control questionnaire (ACQ), serum triacylglycerides and lipid mediator profile in urine and serum.
RESULTS: PD15 (geometric mean, 95% CI) to mannitol following supplementation with omega-3s (78 mg, 51-119) was not different to placebo (88mg, 56-139)(p=0.5). There were no changes in sputum eosinophils (mean±SD) in a sub-group of subjects (omega-3s;8.4±8.2%: placebo;7.8±11.8%,p=0.9)(n=11). At the end of each treatment period there were no differences in FEV1 (% predicted)(omega-3s;85±13%: placebo;84±11%,p=0.9) or ACQ (omega-3s;1.1±0.5%: placebo;1.1±0.5%,p=0.9)(n=23). Omega-3s caused significant lowering of blood triglycerides and expected shifts in serum fatty acids and eicosanoid metabolites, confirming adherence to the supplements; however, no changes were observed in urinary mast cell mediators.
CONCLUSION: Three weeks of omega-3 supplements does not improve BHR to mannitol, decrease sputum eosinophils or inhibit urinary excretion of mast cell mediators in persons with mild-moderate asthma indicating that dietary omega-3 supplementation is not useful in the short-term treatment of asthma.

 

Chest. 2014 Oct 16. doi: 10.1378/chest.14-1214. [Epub ahead of print]


 


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