We would like to thank F. Hargreave and K. Parameswaran for their suggestion that sputum eosinophils and the provocative dose causing a 20% fall in forced expiratory volume in one second (PD20) might reflect partially distinct pathophysiological phenomena 1.
In our study, we did not find a relationship between bronchial hyperresponsiveness (PD20) and the change from baseline of the cough score. This applied to smokers as well as nonsmokers (both p>0.80) 2.
The “increasing evidence” regarding the mechanism of eosinophilic bronchitis refers to small uncontrolled studies 3, 4 or studies in severely obstructive patients 5, 6. In the study by Pizzichine et al. 7, 44 adults (32 nonsmokers), with a daily bothersome cough for ≥1 yr, were included. None of the patients had sputum eosinophilia, and no effect was found of a 2-week treatment with budesonide compared with placebo.
Eosinophilic bronchitis occurs in 10–30% of patients referred to a specialist for chronic cough 8–10, and in 14 out of 82 (17%) primary care patients with cough (mean (range) duration 11 months (1–96)) 11. However, in a subset of 36 patients who responded to budesonide only, seven out of 34 (thus, not more than in the studies mentioned previously) fulfilled the criterion for sputum eosinophilia (>3%) 12.
Interestingly, in our study 2, as well as the study of Rytila et al. 12, cough appears to be at least as sensitive to anti-inflammatory therapy compared with other lower respiratory tract infection symptoms like wheeze and dyspnoea. Nevertheless, we agree with F. Hargreave and K. Parameswaran that the measurement of airway inflammation may help to clarify the mechanism of action of anti-inflammatory medications.
Cough may be a target symptom in studies of the mechanisms of anti-inflammatory treatment for lower respiratory tract symptoms in healthy subjects. The recent literature and the results of our study 2 suggest that investigation of sputum in nonsmoking patients, who present with unexplained cough to their doctor, is feasible and worthwhile.
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