PurposeGrouping COPD subjects into clinical phenotypes might be useful for the management of the disease, but the clinical implications of such classification are still not totally clear, especially regarding prognosis. The primary objective of this study was to assess whether the mortality rates were different between four predefined clinical phenotypes.Patients and methodsThis is a retrospective, observational study carried out at the COPD clinic of a University Hospital. A total of 891 COPD patients were classified, according to the Spanish COPD guidelines, into the following four phenotypes: asthma–COPD overlap (ACO; 75 subjects), nonexacerbator (NONEX; 531 subjects), exacerbator with chronic bronchitis (EXCB; 194 subjects), and exacerbator with emphysema (EXEMPH; 91 subjects). We compared the mortality outcomes between the phenotypes.ResultsAfter a follow-up of 48.4±25.2 months, there were 194 deaths (21.8%). There were significant differences in all-cause mortality between phenotypes. The ACO phenotype had the best long-term prognosis, whereas EXEMPH had the highest risk of death. NONEX and EXCB mortality figures were in between the other two groups. We also found some differences in the causes of death, and patients with EXEMPH were at a higher risk of dying because of COPD itself. The differences in mortality did not seem related to the classification into phenotypes in itself but to disparities in COPD severity and comorbidity load between groups.ConclusionClassifying COPD patients according to several predefined clinical phenotypes can identify clusters of subjects with different mortality outcomes. Some phenotypes are associated with a specific cause of death. The mechanisms that underlie these differences seem to be related to COPD severity and comorbidities.

Background and objectiveIt is known that biomarkers of systemic inflammation are raised in COPD caused by tobacco (T-COPD) compared with healthy controls, but there is less information on the inflammatory status of subjects with COPD caused by biomass smoke (B-COPD). In addition, the possible (if any) differences in inflammation between both types of the disease are still not well known. The aim of this study was to assess the inflammatory profile in B-COPD and T-COPD.MethodsA total of 20 subjects (15 men and five women) with T-COPD were matched one to one for sex, age and forced expiratory volume in 1 s (FEV1) to 20 B-COPD patients. In all, 20 sex-matched healthy subjects with normal lung function without smoking history or biomass exposure were included as controls. The following biomarkers were measured: exhaled nitric oxide, serum IL-6, IL-8, IL-5, IL-13, periostin, surfactant protein-P, TNF-α, IgE, erythrocyte sedimentation rate, C-reactive protein and fibrinogen. Complete blood count was also obtained.ResultsThe age of the subjects was 70.2±7.9 years and FEV1% was 56.2%±14.6%. Most inflammatory biomarkers were higher in both types of COPD than in healthy controls. IL-6, IL-8 and IL-5 were significantly higher in T-COPD than in B-COPD, without other significant differences.ConclusionBoth types of COPD are associated with high levels of systemic inflammation biomarkers. T-COPD patients have a higher systemic inflammatory status than the patients with B-COPD.

Background: Comorbidities are very common in chronic obstructive pulmonary disease (COPD), contributing to the overall severity of the disease. The relative prevalence of comorbidities in COPD caused by biomass smoke (B-COPD), compared with COPD related to tobacco (T-COPD), is not well known. Objectives: To establish if both types of COPD are associated with a different risk for several major comorbidities. Method: The prevalence of comorbidities was compared in 863 subjects with B-COPD (n = 179, 20.7%) or T-COPD (n = 684, 79.2%). Multivariate analysis was carried out to explore the independent relationship between comorbidities and type of exposure. Results: Three comorbidities were more frequent in T-COPD than in B-COPD: ischemic heart disease (11.5 vs. 5.0%, respectively, p = 0.01), peripheral vascular disease (9.2 vs. 2.7%, p = 0.006), and peptic ulcer disease (4.8% vs. 0, p = 0.005). After correcting for potential confounding variables, the risk of ischemic heart disease was lower in B-COPD than in T-COPD (OR: 0.33, 95% CI: 0.16-0.69, p = 0.003). Conclusions: The prevalence of ischemic heart disease is significantly lower in B-COPD than in T-COPD, suggesting a different systemic effect of both types of smoke in COPD patients.

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Multidimensional indices of COPD severity and comorbidity predict all-cause mortality in BS-COPD. The behavior of the different indices is different for BS-COPD and T-COPD.