Kirsch C M, Payan D G, Wong M Y, Dohlman J G, Blake V A, Petri M A, Offenberger J, Goetzl E J, Gold W M
Department of Medicine, University of California, San Francisco 94143.
Clin Allergy. 1988 Mar;18(2):177-87. doi: 10.1111/j.1365-2222.1988.tb02857.x.
The role of arachidonic acid metabolites in the pathogenesis of airway inflammation and clinical asthma is currently unknown. The addition of eicosapentaenoic acid (EPA) to the diet of humans has been shown to generate metabolites that are less potent than their arachidonic acid counterparts. The substitution of EPA for arachidonic acid metabolites in patients might cause a decrease in airway inflammation and an improvement in clinical asthma. We studied the effect of addition of EPA to the diet of twelve asthmatic patients. Standard clinical evaluations and pulmonary function tests were done on weeks 0, 3, 6, 10, 12 and 14. Patients ingested either low-dose EPA (0.1 g/day) or high-dose EPA (4.0 g/day) from weeks 6-14 (total of 8 weeks). There was no difference in clinical status or pulmonary function between groups at the start of the study. There was no change in clinical status or pulmonary function between or within groups at the end of 8 weeks of EPA ingestion.
目前尚不清楚花生四烯酸代谢产物在气道炎症和临床哮喘发病机制中的作用。研究表明,在人类饮食中添加二十碳五烯酸(EPA)会产生比其花生四烯酸对应物活性更低的代谢产物。在患者中用EPA替代花生四烯酸代谢产物可能会导致气道炎症减轻和临床哮喘症状改善。我们研究了在12名哮喘患者的饮食中添加EPA的效果。在第0、3、6、10、12和14周进行了标准临床评估和肺功能测试。从第6 - 14周(共8周),患者分别摄入低剂量EPA(0.1克/天)或高剂量EPA(4.0克/天)。研究开始时,两组之间的临床状况和肺功能没有差异。在摄入EPA 8周结束时,组间或组内的临床状况和肺功能均无变化。