BACKGROUND: Although some non-asthmatic subjects with allergic rhinitis exhibit airway hyperresponsiveness and increased diurnal peak expiratory flow (PEF) variation, little is known about the critical features that determine these physiologic alterations. OBJECTIVE: In subjects with allergic rhinitis and methacholine hyperresponsiveness but no asthma symptoms, we examined whether there were features of asthmatic airway inflammation. METHODS: Forty non-asthmatic adults (11 with allergic rhinitis and methacholine hyperresponsiveness, 20 with allergic rhinitis and normal methacholine responsiveness, and 9 healthy control subjects) were studied. Sputum was induced with inhaled hypertonic saline for 5-minute periods for up to 20 minutes. Plugs from the lower respiratory tract were selected for differential counting in cytocentrifuged preparations. For the next 14 days, subjects measured their PEF two times daily. Peak expiratory flow variation was expressed as amplitude % mean. RESULTS: Peak expiratory flow variation was significantly higher in subjects with allergic rhinitis and methacholine hyperresponsiveness than in allergic rhinitis patients with normal methacholine responsiveness and healthy controls. Eosinophil counts in the induced sputum were significantly higher in the subjects with allergic rhinitis and methacholine hyperresponsiveness [median (interquartile range), 7.3 (9.0)%] compared with allergic rhinitis patients with normal methacholine responsiveness [2.5 (3.8)%, P = .03] and healthy controls [1.0 (1.0)%, P = .02]. CONCLUSION: We conclude that eosinophilic inflammation may be present in subjects with allergic rhinitis and airway hyperresponsiveness even when there are no symptoms of asthma. This could indicate that bronchial eosinophilia is insufficient to cause asthmatic symptoms.
BACKGROUND: Although some non-asthmatic subjects with allergic rhinitis exhibit airway hyperresponsiveness and increased diurnal peak expiratory flow (PEF) variation, little is known about the critical features that determine these physiologic alterations. OBJECTIVE: In subjects with allergic rhinitis and methacholine hyperresponsiveness but no asthma symptoms, we examined whether there were features of asthmatic airway inflammation. METHODS: Forty non-asthmatic adults (11 with allergic rhinitis and methacholine hyperresponsiveness, 20 with allergic rhinitis and normal methacholine responsiveness, and 9 healthy control subjects) were studied. Sputum was induced with inhaled hypertonic saline for 5-minute periods for up to 20 minutes. Plugs from the lower respiratory tract were selected for differential counting in cytocentrifuged preparations. For the next 14 days, subjects measured their PEF two times daily. Peak expiratory flow variation was expressed as amplitude % mean. RESULTS: Peak expiratory flow variation was significantly higher in subjects with allergic rhinitis and methacholine hyperresponsiveness than in allergic rhinitispatients with normal methacholine responsiveness and healthy controls. Eosinophil counts in the induced sputum were significantly higher in the subjects with allergic rhinitis and methacholine hyperresponsiveness [median (interquartile range), 7.3 (9.0)%] compared with allergic rhinitispatients with normal methacholine responsiveness [2.5 (3.8)%, P = .03] and healthy controls [1.0 (1.0)%, P = .02]. CONCLUSION: We conclude that eosinophilic inflammation may be present in subjects with allergic rhinitis and airway hyperresponsiveness even when there are no symptoms of asthma. This could indicate that bronchial eosinophilia is insufficient to cause asthmatic symptoms.