Verleden G M, Dupont L J, Verpeut A C, Demedts M G
Department of Respiratory Diseases, University Hospital Gasthuisberg, Leuven, Belgium.
Chest. 1999 Jul;116(1):59-64. doi: 10.1378/chest.116.1.59.
It has been demonstrated previously that exhaled nitric oxide (eNO) is increased in steroid-naive asthmatics and that inhaled steroids reduce eNO in these patients. Cigarette smoking has also been reported to reduce the eNO in healthy volunteers. Recently a correlation has been demonstrated between eNO and airway hyperresponsiveness in steroid-naive, mild asthmatics. We hypothesized that cigarette smoking would reduce the eNO level in steroid-naive asthmatics and might, therefore, affect the correlation between eNO and airway hyperresponsiveness.
Comparison of eNO in healthy smoking and nonsmoking volunteers with the level of eNO in steroid-naive and steroid-treated asthmatics. Correlate the eNO level with the provocative concentration of histamine causing a 20% fall in FEV1 (PC20hist) in the asthmatic smoking and nonsmoking patients.
University outpatient asthma clinic.
eNO levels and PC20hist were measured in three different asthmatic patient groups (group A = 29 steroid-naive, nonsmoking asthmatics; group B = 19 steroid-treated, nonsmoking asthmatics; and group C = 13 smoking, steroid-naive asthmatics) and in two healthy volunteer groups (group D = 18 nonsmoking; and group E = 16 smoking).
eNO in group A was significantly increased compared with the values in groups B and D (21.8+/-12.7, 12.8+/-4.9, and 10.6+/-2.2 parts per billion [ppb], respectively). Cigarette smoking decreased eNO in healthy volunteers (7.4+/-1.8 ppb, group E) as well as in steroid-naive asthmatics (12.7+/-5.1 ppb, group C). There was a significant correlation between eNO and PC20hist in group A (r = -0.45, p < 0.05); this correlation was, however, lost in both groups B and C.
Cigarette smoking and inhaled steroids reduce the eNO in patients with mild asthma to a comparable extent. Because the correlation between eNO and airway hyperresponsiveness was lost in steroid-treated and smoking, steroid-naive asthmatics, we question the value of eNO as a marker of airway inflammation, at least in mild asthmatics who are already being treated with inhaled steroids or who are currently smoking.
先前已证实，初治哮喘患者呼出一氧化氮（eNO）水平升高，吸入性糖皮质激素可降低这些患者的eNO水平。据报道，吸烟也会降低健康志愿者的eNO水平。最近在初治的轻度哮喘患者中已证实eNO与气道高反应性之间存在相关性。我们推测吸烟会降低初治哮喘患者的eNO水平，因此可能会影响eNO与气道高反应性之间的相关性。
比较健康吸烟和不吸烟志愿者的eNO水平与初治和接受糖皮质激素治疗的哮喘患者的eNO水平。将哮喘吸烟和不吸烟患者的eNO水平与引起第一秒用力呼气容积（FEV1）下降20%的组胺激发浓度（PC20组胺）进行相关性分析。
大学门诊哮喘诊所。
对三组不同的哮喘患者（A组=29例初治、不吸烟的哮喘患者；B组=19例接受糖皮质激素治疗、不吸烟的哮喘患者；C组=13例吸烟、初治的哮喘患者）以及两组健康志愿者（D组=18例不吸烟；E组=16例吸烟）测量eNO水平和PC20组胺。
与B组和D组相比，A组的eNO显著升高（分别为21.8±12.7、12.8±4.9和10.6±2.2十亿分之一[ppb]）。吸烟降低了健康志愿者（E组为7.4±1.8 ppb）以及初治哮喘患者（C组为12.7±5.1 ppb）的eNO水平。A组中eNO与PC20组胺之间存在显著相关性（r=-0.45，p<0.05）；然而，B组和C组中这种相关性均消失。
吸烟和吸入性糖皮质激素在相当程度上降低了轻度哮喘患者的eNO水平。由于在接受糖皮质激素治疗的哮喘患者以及吸烟的初治哮喘患者中，eNO与气道高反应性之间的相关性消失，我们质疑eNO作为气道炎症标志物的价值，至少对于已经接受吸入性糖皮质激素治疗或正在吸烟的轻度哮喘患者而言如此。
