Freezer N J, Croasdell H, Doull I J, Holgate S T
University Medicine, Southampton General Hospital, UK.
Eur Respir J. 1995 Sep;8(9):1488-93.
The role of airway inflammation in the pathogenesis of asthma in childhood is uncertain. In the present study, 27 atopic and nonatopic children aged 7-9 yrs who had > or = 5 episodes of wheeze and symptoms of exercise-induced asthma (EIA) in the previous 12 months, performed a methacholine challenge and exercise test on separate days at monthly intervals. The subjects had not received oral or inhaled corticosteroids for 12 months prior to the study. The dose-response relationship to inhaled methacholine was expressed as the cumulative dose provoking a 20% decrease in forced expiratory volume in one second (PD20). Forced expiratory volume in one second (FEV1) and peak expiratory flow (PEF) were measured prior to the exercise test and at 0, 3, 5, 10, 15 and 20 min following maximal exercise. Following the first methacholine challenge and exercise test, the children were randomized in a double-blind manner to receive inhaled beclomethasone dipropionate (BDP) 200 micrograms b.i.d. or a placebo b.i.d. from a Diskhaler for 3 months. All children were asymptomatic at the time of testing, and there was no significant change in the baseline FEV1 of any subject prior to either challenge throughout the study period. When compared to placebo, the bronchial responsiveness to exercise and methacholine was significantly attenuated in the children who had received inhaled BDP for at least 1 month. There was no relationship between the bronchial responsiveness to methacholine and exercise. There was no significant difference in the bronchial responsiveness to either stimulus in the atopic and nonatopic children. The results of this study suggest that immunoglobulin E (IgE)- and non-IgE-mediated airway inflammation are important in exercise- and methacholine-induced bronchoconstriction in children with recurrent wheeze, although it is probable that different mechanisms are responsible.
气道炎症在儿童哮喘发病机制中的作用尚不确定。在本研究中，27名7至9岁的特应性和非特应性儿童，在过去12个月中有≥5次喘息发作及运动诱发哮喘（EIA）症状，于每月不同日期分别进行了乙酰甲胆碱激发试验和运动试验。在研究前12个月，这些受试者未接受过口服或吸入糖皮质激素治疗。吸入乙酰甲胆碱的剂量-反应关系以引起一秒用力呼气量（FEV1）下降20%的累积剂量（PD20）表示。在运动试验前以及最大运动后0、3、5、10、15和20分钟测量一秒用力呼气量（FEV1）和呼气峰值流速（PEF）。在首次乙酰甲胆碱激发试验和运动试验后，儿童被双盲随机分组，接受来自都保的吸入性二丙酸倍氯米松（BDP）200微克，每日两次，或安慰剂，每日两次，为期3个月。所有儿童在测试时均无症状，且在整个研究期间，任何受试者在任何一次激发试验前的基线FEV1均无显著变化。与安慰剂相比，接受吸入BDP至少1个月的儿童对运动和乙酰甲胆碱的支气管反应性显著减弱。对乙酰甲胆碱的支气管反应性与运动之间无相关性。特应性和非特应性儿童对任何一种刺激的支气管反应性无显著差异。本研究结果表明，免疫球蛋白E（IgE）介导和非IgE介导的气道炎症在复发性喘息儿童的运动和乙酰甲胆碱诱发的支气管收缩中起重要作用，尽管可能是不同机制所致。
