Rolla G, Di Emanuele A, Dutto L, Marsico P, Nebiolo F, Corradi F, Brussino L, Bucca C
Allergologia e Immunologia Cinica, Università di Torino and Ospedale Mauriziano Umberto I di Torino, Largo Turati 62, 10128 Turin, Italy.
Allergy. 2004 Aug;59(8):827-32. doi: 10.1111/j.1398-9995.2004.00502.x.
A complex relationship between arachidonic acid metabolites and nitric oxide (NO) synthesis has been reported in asthma. The effects of inhaled aspirin on fractional exhaled NO (FENO) in patients with aspirin-tolerant (ATA) and aspirin-inducible (AIA) asthma compared with normal controls have been investigated.
The FENO was measured baseline, after saline and lysine-aspirin (L-ASA) bronchial challenge in 10 patients with ATA and in 10 patients with AIA [mean (PD(20)FEV(1) L-ASA): 14.7 +/- 12.7 mg], who had comparable age and baseline FEV(1). Ten healthy subjects served as controls. Sputum eosinophils were counted after saline and after L-ASA challenge in the two groups of asthmatics.
Asthmatic patients had baseline FENO significantly higher than controls (29.7 +/- 6.8 vs 9.8 +/- 2.05 p.p.b. respectively, P < 0.0001). No difference was observed in methacholine PD(20)FEV(1) and baseline FENO between ATA and AIA patients. After L-ASA inhalation, FENO increased significantly only in patients with AIA, reaching the peak value 4 h after bronchoconstriction (from 31.1 +/- 6 to 43 +/- 4.8 p.p.b., P < 0.001), while no change was observed in patients with ATA and in controls. Sputum eosinophils increased significantly after L-ASA inhalation only in patients with AIA (from 8.1 +/- 2.7 to 11.1 +/- 2.8%, P < 0.005) and there was a significant relationship between the increase in sputum eosinophils and the increase in FENO after ASA challenge.
Exhaled NO may indicate eosinophilic airway inflammation during ASA exposure in patients with ASA inducible asthma.
已有报道称哮喘患者体内花生四烯酸代谢物与一氧化氮（NO）合成之间存在复杂关系。本研究调查了吸入阿司匹林对阿司匹林耐受型（ATA）和阿司匹林诱发型（AIA）哮喘患者呼出气一氧化氮分数（FENO）的影响，并与正常对照组进行比较。
对10例ATA患者和10例AIA患者[赖氨酸阿司匹林（L-ASA）激发试验的平均（PD(20)FEV(1) L-ASA）：14.7±12.7 mg]进行基线、盐水激发试验和L-ASA支气管激发试验后FENO的测量，这两组患者年龄和基线FEV(1)相当。10名健康受试者作为对照。对两组哮喘患者在盐水激发试验和L-ASA激发试验后进行痰液嗜酸性粒细胞计数。
哮喘患者的基线FENO显著高于对照组（分别为29.7±6.8 vs 9.8±2.05 ppb，P<0.0001）。ATA患者和AIA患者之间的乙酰甲胆碱PD(20)FEV(1)和基线FENO无差异。吸入L-ASA后，仅AIA患者的FENO显著增加，在支气管收缩后4小时达到峰值（从31.1±6升至43±4.8 ppb，P<0.001），而ATA患者和对照组未观察到变化。仅AIA患者吸入L-ASA后痰液嗜酸性粒细胞显著增加（从8.1±2.7%升至11.1±2.8%，P<0.005），且痰液嗜酸性粒细胞增加与ASA激发试验后FENO增加之间存在显著相关性。
呼出气NO可能表明阿司匹林诱发型哮喘患者在接触阿司匹林期间存在嗜酸性粒细胞性气道炎症。
