RT Journal Article SR Electronic T1 Exhaled NO but not eosinophilic inflammation is reduced by inhaled corticosteroid treatment in COPD JF European Respiratory Journal JO Eur Respir J FD European Respiratory Society SP P719 VO 42 IS Suppl 57 A1 Andrei Malinovschi A1 Gunnar Johansson A1 Per Venge A1 Hans Hedenström A1 Christer Janson A1 Kjell Alving YR 2013 UL http://erj.ersjournals.com/content/42/Suppl_57/P719.abstract AB Exhaled NO (FeNO) is a marker of airways inflammation that relates to eosinophilic inflammation in asthma. A subgroup of subjects with COPD has elevated FeNO levels, but no studies have analysed the relation between FeNO and eosinophilic inflammation in COPD. Therefore, we studied the relation between FeNO and markers of eosinophil activity, as well as their response to inhaled corticosteroid (ICS) treatment, in patients with COPD.FeNO, serum ECP and blood eosinophils (B-Eos) were measured in 36 steroid-naive, ex-smoking patients with COPD, aged 54 to 79 yrs, before and after 4 weeks of treatment with 800 μg mometasone furoate/day in a double-blind, placebo-controlled, crossover study. Patients were grouped as having normal FeNO (<25 ppb) (n=19) and intermediate-increased FeNO (≥25 ppb) (n=17).ECP levels (μg/L, median (IQR)) were similar in both FeNO groups (25 (12.7, 106) vs 44.3 (14.6, 82.9), p=0.60) and no relation was found between serum ECP and FeNO in all subjects (rho=0.04, p=0.82). Similarly, no differences between FeNO groups were found in B-Eos (109/L, median (IQR)) (0.2 (0.1, 0.3) vs 0.2 (0.1, 0.2), p=0.46) nor was any relation found between B-Eos and FeNO in all subjects (rho=-0.17, p=0.32). The decrease of FeNO levels (ppb, median(IQR)) during ICS treatment was significantly larger than during placebo treatment (-4.5 (-11.5, -1) vs 0.8 (-2.3, 6), p=0.008) while no such differences were found for ECP or B-Eos (p=0.35 and p=0.31).In conclusion, exhaled NO did not relate to markers of eosinophilic inflammation in COPD. Furthermore only exhaled NO was decreased by ICS treatment. This suggests a dissociation between exhaled NO and eosinophilic inflammation in COPD.