Abstract
Although the aetiology of chronic cough in guidelines is clearly stated as asthma and related syndromes, gastro-oesophageal reflux disease (GORD), and upper airways disease, the inflammatory mechanisms underlying these conditions differ. Recent studies on asthma have increasingly focused on its molecular phenotypes instead of clinical characteristics. Here, we proposed the hypothesis that divides cough into two groups; the eosinophilic and neutrophilic. This division will enhance our ability to recognise the type of airway inflammation which, as a consequence will lead us to more targeted and personalized treatment approaches.
Highlights
Cough is one of the most common symptoms in respiratory disease which forces patients to seek medical attention
Administration of IL-25 and co-infection of mice with Nippostrongylus brasiliensis [47] and helminth [48] in other studies, revealed similar results. These findings indicated that type2 cytokines and eosinophilia can be produced without the adaptive immune system activation
A systematic review and meta-analysis study in asthma reported that receiver operating characteristics area under the curve (ROC AUC) for fractional exhaled nitric oxide (FeNO) in 17 adult studies (3216 patients) was 0·75
Summary
Cough is one of the most common symptoms in respiratory disease which forces patients to seek medical attention. Many patients report that their chronic cough was preceded by an acute respiratory tract infection suggesting a common mechanism of cough hypersensitivity. Despite following diagnostic algorithms in cough guidelines, in many patients the cause of cough remains obscure leading to term “idiopathic” chronic cough [5, 7, 12, 13] To overcome this diagnostic uncertainty an overarching syndrome based on the observed hypersensitivity to external noxious stimuli was proposed. Evidence for this approach was obtained in a worldwide survey of 10032 chronic cough patients from 11 cough clinics. We suggest that different phenotypes of chronic cough are due to differences in the profile of inflammation seen in individual patients and hypothesise that important therapeutic consequences are dependent on these difference
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