Background Phenotypes of COPD are increasingly recognised, with classification centred on inflammation and in particular microbes and inflammatory markers within the airways and peripheral blood. Studies focusing on eosinophilic inflammation in COPD have shown the validity of airway and peripheral eosinophilia as a marker to direct treatment with corticosteroids. However, the majority of COPD patients have low sputum and peripheral eosinophils, with a large proportion showing raised sputum neutrophils at exacerbation and stable state. The characteristics of this ‘Non-eosinophilic’ group are less well defined, making the identification of biomarkers and target pathways for drug development more challenging.
Methods Baseline data from patients with COPD, previously recruited to a study identifying biomarkers was analysed using SPSS (SPSS version 22, IBM Corp, released 2013, Armonk, NY). A cut off of 3% sputum eosinophils was used to distinguish ‘Eosinophilic’ and ‘Non-eosinophilic’ groups. Parametric and non-parametric analyses were performed where appropriate.
Results Of 149 patients, 96 had <3% sputum eosinophils, with a median age of 69.5 years (47–88 range). There were no differences in gender and proportion of smokers between the two groups. There was an increase in percentage sputum neutrophils in the non-eosinophilic group (mean difference 15%, 95% confidence interval 9–17%, p = 0.01). The non-eosinophilic patients had more exacerbations/person/year compared to the eosinophilic group (3.52 vs. 3.11); this was independent of inhaled corticosteroid use. There were more significant co-morbidities in the non-eosinophilic group compared to the non-eosinophilic group (78% vs. 61%, p < 0.01). Co-morbidity was defined as the presence of cardiovascular disease, endocrine disorders, depression, or musculoskeletal disease.
There were more positive sputum cultures in the non-eosinophilic group compared to the eosinophilic group (33% vs. 11%, p = 0.16). There was also an increase in colony forming units in the non-eosinophilic group compared to the eosinophilic group (mean fold difference 0.4, 95% CI 0–0.8, p = 0.05).
Conclusions Non-eosinophilic COPD subjects have more exacerbations, with more co-morbidities and bacterial burden (see Figure 1). Further work is required to understand the pathogenesis of this phenotype.
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