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Cottingham, UK
Dr. Morice is Professor of Respiratory Medicine, Head of the Division of Academic Medicine, Castle Hill Hospital.
Correspondence to: Alyn H Morice, Professor of Respiratory Medicine, Head of Division of Academic Medicine, Castle Hill Hospital, Castle Rd, Cottingham, East Yorkshire, HU16 5JQ UK; e-mail: a.h.morice{at}hull.ac.uk
On page 362 of this issue of CHEST, Richard Irwin and colleagues1 provide evidence of the histologic changes seen in the airways of patients with chronic cough. They detail the altered morphology present in this syndrome, which includes epithelial denudation, goblet cell and squamous cell metaplasia, and a characteristic mild-to-moderate chronic inflammatory infiltrate with lymphocytes and plasma cells. Evidence of acute inflammation is absent, and there is a lack of eosinophilic inflammation. This clearly differentiates these patients with chronic cough from those with asthma. Obviously, this is not to say that patients with cough-variant asthma or eosinophilic bronchitis do not have T-helper cell type 2 inflammation. The incidence of these asthma-like syndromes varies considerably in reports from specialist cough clinics.2 Instead, it infers that this relatively small sample size did not include a subgroup of chronic coughers with the characteristic histologic pattern of mast cell/eosinophilic inflammation around airway nerves rather than around smooth muscle, which is seen in patients with asthmatic cough.3
The authors then look at the diagnostic subdivisions of chronic cough and, because the histologic changes are uniformly distributed within each group of chronic coughers, conclude, not unreasonably, that these changes are due to the effects of coughing rather than to the effects of any specific change that is the result of different etiologies of cough. While some of the histologic changes such as epithelial denudation may plausibly be ascribed to this mechanism, there is an alternative explanation that bears consideration. The different diagnostic categories within cough are relatively loosely defined, leading, as previously stated, to a marked difference in the relative frequency of the various diagnostic categories. In particular, postnasal drip syndrome (PNDS), or rather, after its renaming in the recent American College of Chest Physicians guidelines4 to the catchy "upper airways cough syndrome," differs markedly, particularly on the two sides of the Atlantic. Even by European standards,5 however, my own opinion that the vast majority of cases of nonasthmatic chronic cough are due to reflux is at the extreme end of the spectrum. In this view, most of the sensation of PNDS is due to extraesophageal non-acid reflux and its consequences. The findings of this present study of a uniformity of response within the airways is supported by studies that have found no difference in levels of inflammatory markers in induced sputum samples67 and neuropeptides8 between the supposedly different etiologies of cough. In the absence of sensitive and specific diagnostic tests (there is no dripometer), the response to "specific" therapy has been used as a surrogate. While a response to therapy with a proton pump inhibitor may be expected to predict a reflux cough since proton pumps are only located in the gastric mucosa, a response to therapy with poorly characterized first-generation antihistamines cannot be regarded as specific. Indeed, we have recently demonstrated9 that the American College of Chest Physicians recommended treatment for PNDS, brompheniramine, is a potent antagonist of the TRPV1 capsaicin receptor, which is a prime candidate for the pharmacologic cough receptor. Thus, brompheniramine is a highly effective but nonspecific antitussive agent, and a response is certainly not diagnostic of PNDS.
Whether the histologic changes seen by Irwin and colleagues1 are specific for chronic cough or specific for coughing could be differentiated in other cough syndromes, such as Tourette syndrome, where the airway is clearly not the primary cause. The histologic demonstration of the unique inflammatory profile in chronic cough is a valuable contribution to our knowledge.
Footnotes
The author has no conflict of interest on this topic.
References
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