TY - JOUR T1 - Markers of airway inflammation and airway hyperresponsiveness in patients with well-controlled asthma JF - European Respiratory Journal JO - Eur Respir J SP - 444 LP - 450 DO - 10.1183/09031936.01.00058601 VL - 18 IS - 3 AU - J.D. Leuppi AU - C.M. Salome AU - C.R. Jenkins AU - H. Koskela AU - J.D. Brannan AU - S.D. Anderson AU - M. Andersson AU - H.K. Chan AU - A.J. Woolcock Y1 - 2001/09/01 UR - http://erj.ersjournals.com/content/18/3/444.abstract N2 - In steroid-naïve asthmatics, airway hyperresponsiveness correlates with noninvasive markers of airway inflammation. Whether this is also true in steroid-treated asthmatics, is unknown.In 31 stable asthmatics (mean age 45.4 yrs, range 22–69; 17 females) taking a median dose of 1,000 µg inhaled corticosteroids (ICS) per day (range 100–3,600 µg·day−1), airway responsiveness to the “direct” agent histamine and to the “indirect” agent mannitol, lung function (forced expiratory volume in one second (FEV1), forced vital capacity (FVC), peak expiratory flow (PEF)), exhaled nitric oxide (eNO), and number of inflammatory cells in induced sputum as a percentage of total cell count were measured.Of the 31 subjects, 16 were hyperresponsive to mannitol and 11 to histamine. The dose-response ratio (DRR: % fall in FEV1/cumulative dose) to both challenge tests was correlated (r=0.59, p=0.0004). However, DRR for histamine and DRR for mannitol were not related to basic lung function, eNO, per cent sputum eosinophils and ICS dose. In addition, NO was not related to basic lung function and per cent sputum eosinophils.In clinically well-controlled asthmatics taking inhaled corticosteroids, there is no relationship between markers of airway inflammation (such as exhaled nitric oxide and sputum eosinophils) and airway responsiveness to either direct (histamine) or indirect (mannitol) challenge. Airway hyperresponsiveness in clinically well-controlled asthmatics appears to be independent of eosinophilic airway inflammation.Supported by the National Health and Medical Research Council, the Australian ARDS Association, and a grant-in aid from Rhone-Poulenc Rorer, Australia. J. Leuppi was funded by Swiss National Science Foundation; Novartis-Foundation, Switzerland; and Swiss Respiratory Society. ER -