Bronchial responsiveness and airway inflammation in patients with nonallergic rhinitis with eosinophilia syndrome

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Abstract

Background: Nonallergic rhinitis with eosinophilia syndrome (NARES) is characterized by persistent nasal symptoms without allergy and by a marked eosinophil recruitment in the nasal cavities. Objective: We studied whether patients with NARES had bronchial responsiveness to methacholine and airway inflammation and examined the relationship between these factors. Methods: We selected a group of 39 patients referred to our allergy clinic for symptoms of perennial rhinitis. Atopic status was excluded by skin prick tests and RASTs. None of the patients had a history of respiratory symptoms. We preliminarily performed nasal lavage in all patients, and the diagnosis of NARES was made on the basis of the presence of at least 10% eosinophils in nasal lavage fluid. A methacholine challenge and sputum induction were also done on two different days. Results: Eosinophils in nasal lavage fluid ranged between 10% and 86%. Serum IgE levels were within normal range. Total circulating eosinophils ranged between 40 and 890/mm3. Methacholine PD20 values were measurable in only 18 patients (range, 0.32 to 22.56 μmol; group 1). In the remaining 21 patients, methacholine PD20 values were greater than 24 μmol (group 2). We found that differential cell counts in nasal lavage fluid in group 1 were not different from those in group 2. Methacholine PD20 values were not significantly related to any cell count in the nasal lavage fluid. Induced sputum was accomplished only in 22 patients. Eosinophils in induced sputum ranged between 0% and 56.5%. Numbers of total cells, macrophages, lymphocytes, neutrophils, and epithelial cells in the two subgroups were not different. The number of metachromatic cells tended to be higher in group 1 compared with group 2 (0.31% vs 0.05%), but the difference was not significant. The eosinophil count in the induced sputum was significantly higher in group 1 compared with group 2 (16.8% vs 3.1%; p < 0.05). In the entire population, methacholine PD20 values were significantly correlated with the number of eosinophils in sputum (r = –0.63; p < 0.001). Conclusion: We showed that 46% of patients with NARES but without histories of respiratory symptoms had a measurable bronchial responsiveness. The presence of bronchial responsiveness was associated with an increased number of eosinophils in induced sputum but not with the inflammatory process in the nose. (J Allergy Clin Immunol 1997;100:775-80.)

Section snippets

Population

We studied 39 patients between November 1993 and April 1995 referred to our outpatient clinic on the basis of a history of perennial rhinitis. All patients lived in a highly polluted area (Milan, northern Italy). Patients were selected if they matched the following criteria: negative responses to skin prick tests with extracts of 16 common airborne allergens; negative RAST results; levels of total serum IgE within the normal range; absence of any history of respiratory symptoms, including

RESULTS

The clinical and functional characteristics of the entire population are shown in Table I.

. Physiologic and clinical characteristics of patients

Entire population (N =39)Group 1 (N=18)Group 2 (N = 21)
Sex (M/F)13/264/149/12
Age (yr)35.7 ± 2.1 (17-67)36.4 ± 3.6 (19-67)35.2 ± 2.5 (17-58)
Length of clinical history (yr)3.3 ± 0.7 (0.3-20)1.8 ± 0.4 (0.3-6)4.5 ± 1.3* (0.3-20)
FEV1 (percent predicted)98.1 ± 2.0 (60-121)91.3 ± 1.8 (75-102)104.0 ± 2.9† (60-121)
Blood eosinophils (cells/mm3)350.6 ± 40.2 (40-890)

DISCUSSION

This study demonstrated that bronchial responsiveness is measurable in approximately 46% of patients with NARES and that there is clear evidence for the presence of bronchial inflammation in patients with NARES. We observed that the mean percentage of eosinophils in induced sputum is significantly higher in patients with measurable methacholine PD20 values compared with that found in patients without bronchial responsiveness.

NARES has been defined on the basis of the presence of persistent

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    Reprint requests: Antonio Foresi, MD, Servizio di Fisiopatologia Respiratoria, Viale Matteotti 83, 20099 Sesto San Giovanni, Italy.

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