Eosinophilic airway inflammation in nasal polyposis

Background: Asthma and asymptomatic bronchial hyperresponsiveness (BHR) are frequent findings in patients with nasal polyposis (NP), Objective: To elucidate mechanisms responsible for the development of BHR, we initiated a prospective study of bronchial inflammation as assessed by b ronchial lavage (BL) and bronchial biopsy specimens in 35 patients with non infectious NP. Methods: BHR was determined with methacholine provocation testing. Differen tial cell count, ECP, and histamine and tryptase levels were determined in BLs, Pathologic examination of bronchial biopsy specimens was performed wit h May-Grunwald-Giemsa stain to assess the number of lymphocytes, Indirect i mmunoenzymatic methods were used to identify eosinophils and mast cells, Results: Fourteen patients did not exhibit BHR (group A); 7 patients had as ymptomatic BHR (group B); and 14 patients had BHR associated with asthma (g roup C), Patients of group C tended to have a longer duration of nasal symp toms than those of groups A and B. FEV1 (L) was significantly lower in grou p C than in groups A and B, The number and percentage of eosinophils were s ignificantly higher in BLs in groups B and C than in group A (P <.05). Pati ents of groups B and C had a significantly higher number of eosinophils in bronchial submucosa (14.0 +/- 1.5/mm(2) and 19.0 +/- 1.9/mm(2), respectivel y) than patients of group A (0.1 +/- 0.1/mm(2)). The number of lymphocytes was also higher in groups B and C than in group A. FEV1 (percent of predict ed value) and eosinophil number within bronchial mucosa correlated negative ly. Conclusion: Our results demonstrate that patients with NP and asymptomatic BHR had an eosinophilic bronchial inflammation similar to that observed in asthmatic patients with NP, whereas patients with NP without BHR do not fea ture eosinophilic lower airways inflammation. The clinical relevance of the se results requires careful follow-up to determine whether eosinophilic inf lammation in these patients precedes and is responsible for the development of obvious asthma.