Non-invasive markers of airway inflammation as predictors of oral steroid responsiveness in asthma

Citation
Sa. Little et al., Non-invasive markers of airway inflammation as predictors of oral steroid responsiveness in asthma, THORAX, 55(3), 2000, pp. 232-234
Citations number
10
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
THORAX
ISSN journal
00406376 → ACNP
Volume
55
Issue
3
Year of publication
2000
Pages
232 - 234
Database
ISI
SICI code
0040-6376(200003)55:3<232:NMOAIA>2.0.ZU;2-Y
Abstract
Background-Sputum eosinophil counts and exhaled nitric oxide (NO) levels ar e increased in asthma and both measurements fall in response to corticoster oids. Methods-Exhaled NO levels and sputum eosinophil counts were assessed as non invasive markers of the response to an oral steroid in 37 patients (19 wome n) with stable chronic asthma (mean (SD) age 48.6 (12.2) years, asthma dura tion 25.9 (17.3) years, and baseline forced expiratory volume in one second (FEV1) 76.3 (21.9)% predicted). Spirometric tests, with reversibility to a beta agonist (2.5 mg nebulised salbutamol), and induced sputum (using nebu lised 3% saline) were performed at recruitment and following treatment with 30 mg prednisolone/day for 14 days. Results-Baseline NO levels correlated with the percentage improvement in FE V, from baseline to the post-steroid, postbronchodilator value (r(s) = 0.47 , p = 0.003), with an NO level of >10 ppb at baseline having a positive pre dictive value of 83% for an improvement in FEV, of greater than or equal to 15% (sensitivity 59%, specificity 90%). Sputum eosinophilia (greater than or equal to 4%) had a positive predictive value of 68% (sensitivity 54%, sp ecificity 76%) for an increase in FEV1 of greater than or equal to 15%. A c ombination of sputum eosinophilia and increased NO levels resulted in a pos itive predictive value of 72% and a negative predictive value of 79% (sensi tivity 76%, specificity 75%). Conclusion-Exhaled NO levels and sputum eosinophilia may be useful in predi cting the response to a trial of oral steroid in asthma.