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Sputum eosinophils and bronchodilator reversibility-chronic obstructive pulmonary disease or asthma?
Reversibility of bronchoconstriction in COPD is NOT related to specific inflammation in sputum
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Graeme P Currie Department of Respiratory Medicine, Aberdeen Royal Infirmary, Aberdeen AB25 2ZN, Scotland, UK, Prasima Srivastava, Daniel K C Lee
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graeme.currie{at}nhs.net Graeme P Currie, et al.
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To the Editor: The study by Perng et al (1) evaluated the inflammatory cell constituent and bronchodilator reversibility of a group of patients (n = 88) with stable chronic obstructive pulmonary disease (COPD). The authors concluded that eosinophils play a role in COPD and that along with assessment of bronchodilator reversibility, this knowledge can help tailor pharmacotherapy targeted towards the airways of such individuals. Several points are worthy of mention regarding the selection of patients included in their study, all of whom had a significant smoking history. For example, the authors mentioned that part of their diagnostic criteria included the observation of symptoms of “progressive breathlessness, productive cough and occasional wheezing”. While undoubtedly these features are consistent with COPD, they are far from specific and such symptoms are frequently found in asthma and other respiratory and non-respiratory disorders. Patients in the “bronchodilator reversible” group demonstrated mild airflow limitation with a mean forced expiratory volume in 1 second (FEV1) of 54% predicted – consistent with either COPD or asthma. (2) However, with mean bronchodilator reversibility of 22%, it is pertinent to consider whether these were truly patients with COPD. Indeed, by definition airflow limitation tends to be fixed in COPD, rather than demonstrate significantly reversibility.(2) Moreover, it is noted in the same group of patients that the median sputum eosinophil count was as high as 8%. It would also have been of interest if the authors had measured the gas transfer co-efficient, which if impaired, would have provided more convincing evidence of alveolar damage frequently found in COPD but not in asthma. The results of the study therefore have to be taken lightly, in view of the highly questionable diagnosis of COPD. Moreover, if in fact the patients with significant reversibility and raised eosinophil count indeed had asthma – which may well have been the case (irrespective of smoking history) – it is certainly of grave concern that anti-inflammatory therapy with inhaled corticosteroids was not being instituted. Graeme P Currie, MD Prasima Srivastava, MD Daniel K C Lee, MD † Department of Respiratory Medicine, Aberdeen Royal Infirmary, Foresterhill, Aberdeen AB25 2ZN, Scotland, United Kingdom. † Department of Respiratory Medicine, Ipswich Hospital, Heath Road, Ipswich IP4 5PD, England, United Kingdom. References 1. Perng DW, Huang HY, Chen HM, et al. Characteristics of Airway Inflammation and Bronchodilator Reversibility in COPD: A Potential Guide to Treatment. Chest 2004;126:375-81. 2. National clinical guideline on management of chronic obstructive pulmonary disease in adults in primary and secondary care. Thorax 2004; 59 (suppl 1):1-232. |
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Frans H. Krouwels, pulmonologist OLVG Hospital, Amsterdam, The Netherlands
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F.H.Krouwels{at}olvg.nl Frans H. Krouwels
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The heterogeneity of the population of patients with COPD is an intriguing phenomenon, especially in the context of the efficacy of inhaled corticosteroids in these patients. In the august issue of Chest, Perng et al addressed this issue in a nicely performed study in nonatopic COPD patients with a smoking history who had not taken either oral or inhaled corticosteroids for at least 3 months (1). Patients with a reversible obstruction were compared with non-reversible COPD patients and with healthy controls. They found elevated sputum IL-8 levels in patients with nonreversible obstruction as compared to reversible obstruction, which led them to speculate upon the role of IL-8 in COPD. However, elevated IL-8 levels in the sputum of patients with irreversible airways obstruction may not be a specific phenomenon, but merely the result of increased leakage of proteins into the airway lumen as also sputum albumin was elevated. Increased local albumin as a sign of airway permeability was repeatedly found, not only in patients with COPD but also in asthmatic patients (2,3). The close correlation between sputum IL-8 and albumin levels and the similar ratio IL-8/albumin in both groups suggest that respiratory membrane leakage is the main factor to explain elevated IL-8 levels and not a specific inflammatory parameter. The two COPD populations were not different with respect to sputum eosonophilia. In addition, Perng et al. reported that there was no correlation between airway reversibility and sputum eosinophilia. It is therefore surprising that in the accompanying editorial much attention is given to a supposedly reported relation between bronchodilator reversibility and sputum eosinophilia (4). Even practical and therapeutical implications of this supposed finding are discussed. These conclusions are not supported by the published data. Therefore the finding of sputum eosinophilia in a subpopulation of COPD patients, as was also shown by others (5,6), is intriguing especially in the context of the Dutch hypothesis, but the study of Perng was not able to show a more asthma-like phenotype in these patients. References 1. Perng DW, Huang HY, Chen HM et al. Characteristics of Airway Inflammation and Bronchodilator Reversibility in COPD. Chest 2004;126:375- 381.) 2. Bonomo L, D’Addabo A. [131I] Albumin turnover and loss of protein into the sputum of chronic bronchitis. Clin Chim Acta 1964; 10: 214-22. 3. Schoonbrood DF, Lutter R, Habets FJ. Et al.Analysis of plasma-protein leakage and local secretion in sputum from patients with asthma and chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 1994;150:1519-27. 4. Jindal SK. Dutch hypothesis. Revisited? Chest 2004; 126: 329-331. 5. Saetta M, Stefano AD, Maestrelli P et al. Airway eosinophilia in chronic bronchitis during exacerbation. Am J Respir Crit Care Med 1994; 150: 1646-52. |
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