Article Text

Download PDFPDF

Chronic cough
  1. Department of Respiratory Medicine
  2. Glenfield Hospital NHS Trust
  3. Groby Road, Leicester
  4. LE3 9QP, UK
  2. L G HEANEY,
  3. M ENNIS,
  1. Department of Respiratory Medicine
  2. Belfast City Hospital
  3. Lisburn Road
  4. Belfast BT9 7AB
  5. UK
  1. Friedrichsdorfer Strasse 11
  2. 61352 Bad Homburg
  3. Germany
  4. Krankenhaus Maingau
  5. Scheffelstrasse 2–16
  6. 60318 Frankfurt
  7. Main
  8. Germany

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

McGarvey et al have described the causes of cough and the predictive values of appropriate diagnostic tests in a group of patients presenting to a specialist clinic.1 They have used a histamine challenge test to support the diagnosis of asthma and to justify a trial of inhaled corticosteroid therapy. We agree with the authors’ conclusion that a negative histamine challenge effectively rules out asthma as the cause of chronic cough, but disagree that this obviates the need for a trial of inhaled corticosteroids. Eosinophilic bronchitis presents with a chronic cough and sputum eosinophilia, but without the variable airflow obstruction or airway hyperresponsiveness seen in asthma.2In common with asthma and in contrast to patients with cough without sputum eosinophilia, the cough improves with inhaled corticosteroid therapy. Eosinophilic bronchitis can only be diagnosed if airway inflammation is assessed.

We have prospectively looked for evidence of eosinophilic bronchitis in new patients referred over a two year period with isolated chronic cough.3 Patients were investigated using a standard protocol similar to that suggested by McGarvey et al with the addition of induced sputum. Eosinophilic bronchitis was diagnosed if patients had no symptoms suggesting variable airflow obstruction, normal spirometric values, normal PEF variability, a methacholine provocation concentration causing a 20% fall in FEV1 (PC20) of >8 mg/ml, and a sputum eosinophilia (>3% non-squamous cells). Ninety one patients with chronic cough were identified out of a total of 856 new referrals (10.6%). The primary diagnosis was eosinophilic bronchitis in 12 (13.2%). All improved after treatment with inhaled budesonide 400 μg twice daily and in eight who had a follow up sputum analysis the eosinophil count decreased significantly from 16.8% to 1.6%.

The important practical implication of our findings is that a significant proportion of patients with corticosteroid responsive cough have normal airway responsiveness and no other features of asthma. We suggest that a trial of inhaled corticosteroid therapy, preferably after an assessment of airway inflammation, should be part of the diagnostic algorithm of chronic cough, whether there is hyperresponsiveness or not.


authors’ reply We welcome the comments of Drs Brightling and Pavord. The assessment of airway inflammation using induced sputum is not currently a routine part of our diagnostic algorithm. The data presented by Pavord et al suggest that our group of patients should have included approximately six patients with eosinophilic bronchitis. Since all our patients with a negative histamine challenge responded to treatment either for postnasal drip syndrome (PNDS) or gastro-oesophageal reflux (GOR), or failed to respond to any treatment including inhaled steroids (idiopathic coughers), we feel it unlikely that patients with steroid responsive cough were missed.

We do, however, recognise the concept of airway inflammation in non-asthmatic coughers and currently have an article in press1-1 in which we report that eosinophil numbers are significantly increased in bronchoalveolar lavage fluid from patients with GOR compared with controls. This was not the case for patients with PNDS or idiopathic cough. All the patients with GOR had resolution of cough with acid suppression therapy. Although bronchoalveolar lavage fluid findings may not be directly comparable to induced sputum findings, we suggest that not all patients with chronic cough and a predominant eosinophil component to their airway inflammation require a trial of inhaled steroids.

We agree that assessment of airway inflammation should be considered when evaluating patients with chronic cough and induced sputum may prove to be the best technique. However, it does require certain expertise which may not be readily available in all units encountering patients with chronic cough. Furthermore, airway inflammation is a dynamic process and sampling at one time point only may not reflect relevant airway events. In addition, there may be difficulties in interpreting the cellular profile in induced sputum as evidenced by analysis of samples obtained from mild asthmatics during exacerbations.1-2


  1. 1-1.
  2. 1-2.

We read with great interest the article by McGarveyet al 2-1 concerning the evaluation of patients with non-productive cough. Nowadays “chronic cough” is a well established, uniformly defined entity both in the English and German literature.2-2 Its relation to gastro-oesophageal reflux disease (GERD) is generally acknowledged. The reader may be interested in a very early description of this entity by Thomas Mann in his novel “Buddenbrooks” published in 1901 (Nobel Prize 1929), Volume 1, Part 6, chapter X, translated by H T Lowe-Porter in 1996 (Minerva paperback edition, Mandarin Paperbacks, London): “Never”, she (Tony Buddenbrook) said. And she gave a long audible outward breath and cleared her throat, also at length and deliberately. It was like a dry cough which had of late become almost a habit with her, and had probably to do with her digestive trouble (in German “Magenleiden” = gastric suffering).

By his persistent interest in medical issues, particularly tuberculosis, and his famous expertise in observing individuals, the novelist may have become the first to describe “chronic cough” due to GERD.


  1. 2-1.
  2. 2-2.