Mondino Chiara, Ciabattoni Giovanni, Koch Pierluigi, Pistelli Riccardo, Trové Andrea, Barnes Peter J, Montuschi Paolo
Department of Immunodermatology, Istituto Dermopatico dell'Immacolata, IDI, IRCCS, Rome.
J Allergy Clin Immunol. 2004 Oct;114(4):761-7. doi: 10.1016/j.jaci.2004.06.054.
Lipid mediators play an important pathophysiologic role in atopic asthmatic children, but their role in the airways of atopic nonasthmatic children is unknown.
We sought (1) to measure leukotriene (LT) E 4 , LTB 4 , 8-isoprostane, prostaglandin E 2 , and thromboxane B 2 concentrations in exhaled breath condensate in atopic asthmatic and atopic nonasthmatic children; (2) to measure exhaled nitric oxide (NO) as an independent marker of airway inflammation; and (3) to study the effect of inhaled corticosteroids on exhaled eicosanoids.
Twenty healthy children, 20 atopic nonasthmatic children, 30 steroid-naive atopic asthmatic children, and 25 atopic asthmatic children receiving inhaled corticosteroids were included in a cross-sectional study. An open-label study with inhaled fluticasone (100 microg twice a day for 4 weeks) was undertaken in 14 steroid-naive atopic asthmatic children.
Compared with control subjects, exhaled LTE 4 ( P <.001), LTB 4 ( P <.001), and 8-isoprostane ( P <.001) levels were increased in both steroid-naive and steroid-treated atopic asthmatic children but not in atopic nonasthmatic children (LTE 4 , P=.14; LTB 4 , P=.23; and 8-isoprostane, P=.52). Exhaled NO levels were increased in steroid-naive atopic asthmatic children ( P <.001) and, to a lesser extent, in atopic nonasthmatic children ( P <.01). Inhaled fluticasone reduced exhaled NO (53%, P <.0001) and, to a lesser extent, LTE 4 (18%, P <.01) levels but not LTB 4 , prostaglandin E 2 , or 8-isoprostane levels in steroid-naive asthmatic children. Conclusions Exhaled LTE 4 , LTB 4 , and 8-isoprostane levels are increased in atopic asthmatic children but not in atopic nonasthmatic children. In contrast to exhaled NO, these markers seem to be relatively resistant to inhaled corticosteroids.
脂质介质在特应性哮喘儿童中发挥着重要的病理生理作用，但它们在特应性非哮喘儿童气道中的作用尚不清楚。
我们旨在（1）测量特应性哮喘儿童和特应性非哮喘儿童呼出气冷凝物中白三烯（LT）E4、LTB4、8-异前列腺素、前列腺素E2和血栓素B2的浓度；（2）测量呼出气一氧化氮（NO）作为气道炎症的独立标志物；（3）研究吸入糖皮质激素对呼出气类花生酸的影响。
一项横断面研究纳入了20名健康儿童、20名特应性非哮喘儿童、30名未使用过类固醇的特应性哮喘儿童和25名正在接受吸入糖皮质激素治疗的特应性哮喘儿童。对14名未使用过类固醇的特应性哮喘儿童进行了一项吸入氟替卡松（每日2次，每次100μg，共4周）的开放标签研究。
与对照组相比，未使用过类固醇和使用过类固醇治疗的特应性哮喘儿童呼出气中LTE4（P<.001）、LTB4（P<.001）和8-异前列腺素（P<.001）水平均升高，但特应性非哮喘儿童未升高（LTE4，P=.14；LTB4，P=.23；8-异前列腺素，P=.52）。未使用过类固醇的特应性哮喘儿童呼出气NO水平升高（P<.001），特应性非哮喘儿童呼出气NO水平也有一定程度升高（P<.01）。吸入氟替卡松可降低未使用过类固醇的哮喘儿童呼出气NO水平（53%，P<.0001），并在较小程度上降低LTE4水平（18%，P<.01），但对LTB4、前列腺素E2或8-异前列腺素水平无影响。结论：特应性哮喘儿童呼出气中LTE4、LTB4和8-异前列腺素水平升高，而特应性非哮喘儿童未升高。与呼出气NO不同，这些标志物似乎对吸入糖皮质激素相对不敏感。
