Mast cells and eosinophils may play a role in the pathophysiology of chroni
c cough in nonasthmatics. It is unknown, how;ever, whether degranulation of
these cells occurs in the airways of such patients.
Thirty-five nonsmoking patients referred with a chronic nonproductive cough
(mean cough duration 76.2 months) were evaluated using a comprehensive dia
gnostic protocol. Bronchoalveolar lavage (BAL) cell differentials and BAL h
istamine, tryptase and eosinophilic cationic protein (ECP) concentrations w
ere determined. Ten nonsmoking healthy volunteers served as controls.
Diagnostic subgroups were identified: eight postnasal drip syndrome (PNDS),
seven cough variant asthma (CVA), seven gastro-oeseophageal reflux (GOR),
seven dual aetiology and sis idiopathic, Nonasthmatic coughers (NAC) were c
haracterized as those patients without bronchial hyperresponsiveness on his
tamine challenge and whose cough had either responded to therapy for PNDS o
r GOR or failed to improve with antiasthma therapy. There was a significant
increase in both eosinophil and mast cell numbers (p<0.05) and in histamin
e levels (p= 0.027) when NAC patients were compared with controls, Tryptase
and ECP levels were elevated in 7 of 23 and 6 of 23 NAC patients, respecti
vely.
In conclusion, airway inflammatory cell numbers are not only increased but
also activated, suggesting an important role for airways inflammation in th
e pathophysiology of chronic nonproductive cough.