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1 Institute of Respiratory Medicine, University of Sydney, New South Wales, and 2 Dept of Respiratory Medicine, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia. 4 Died February 17, 2001
CORRESPONDENCE: J.D. Leuppi, Dept of Internal Medicine, University Hospital, CH-4031, Basel, Switzerland. Fax: 41 61265 5353
Keywords: airway hyperresponsiveness, airway inflammation, asthma, exhaled nitric oxide, sputum, steroids
Received: June 28, 2000
Accepted March 20, 2001
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.
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.
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