@article{oai:kanazawa-u.repo.nii.ac.jp:00013678,
 author = {Ishiura, Yoshihisa and Fujimura, Masaki and Yamamoto, Hiroki and Ohkura, Noriyuki and Myou, Shigeharu},
 issue = {11},
 journal = {Cough},
 month = {Jan},
 note = {Background: Sinobronchial syndrome is a cause of chronic productive cough. Inflammatory mediators are involved in the pathophysiology of chronic productive cough. Accumulating evidences indicate that cyclooxygenase (COX)-2, one of the inducible isoforms of COX, is a key element in the pathophysiological process of a number of inflammatory disorders. However, little is known about the role of COX-2 in chronic productive cough in patients with sinobronchial syndrome known as neutrophilic bronchial inflammation.Methods: The effect of etodolac, a potent COX-2 inhibitor, on cough response to inhaled capsaicin was examined in 15 patients with sinobronchial syndrome in a randomized, placebo-controlled cross-over study. Capsaicin cough threshold, defined as the lowest concentration of capsaicin eliciting five or more coughs, was measured as an index of airway cough reflex sensitivity.Results: The cough threshold was significantly (p < 0.03) increased after two-week treatment with etodolac (200 mg twice a day orally) compared with placebo [37.5 (GSEM 1.3) vs. 27.2 (GSEM 1.3) μM].Conclusions: These findings indicate that COX-2 may be a possible modulator augmenting airway cough reflex sensitivity in patients with sinobronchial syndrome. © 2010 Ishiura et al; licensee BioMed Central Ltd.},
 title = {Role of COX-2 in cough reflex sensitivity to inhaled capsaicin in patients with sinobronchial syndrome},
 volume = {6},
 year = {2011}
}