Abstract

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) considers blood eosinophil counts< 100 cells/μL (BEC≤100) in people with COPD to predict poor inhaled corticosteroid (ICS) responsiveness. However, the BEC≤100 phenotype is inadequately characterized, especially in advanced COPD. Are there differences between GOLD group D patients with high BEC and those with low BEC regarding baseline characteristics and longitudinal outcomes? We used multivariable mixed models and logistic regression to contrast clinical characteristics and outcomes of BEC≤100 vsBEC > 100 (BEC100+) in all subjects with COPD (n= 1,414) and GOLD group D subjects (n= 185) not receiving ICS. We identified n= 485 with BEC≤100 (n= 61 GOLD group D) and n= 929 people with BEC100+ (n= 124 GOLD group D). BEC≤100 status was stable at 6weeks and approximately 52weeks (intraclass correlations of 0.78 and 0.71, respectively). Compared with BEC100+, BEC≤100 comprised more women, with greater current smoking, and less frequent childhood asthma. Among all analyzed participants, the two BEC-defined subsets showed similar rates of lung function decline (mean slope, BEC≤100 vsBEC100+, -50 vs-39mL/y; P= .140), exacerbations (0.40 vs0.36/y; P= .098), subsequent ICS initiation (2.5%vs4.4%; P= .071), and mortality (7.8%vs8.4%; P= .715). However, in GOLD group D, people with BEC≤100 showed higher exacerbation rates within 365days of enrollment (0.62 vs0.33/y; P= .002) and total follow-up (1.16 vs0.83/y; P= .014). They also had greater lung function decline (mean slope of -68mL/y vs-23mL/y; P= .036) and had greater emphysema at baseline (voxels< 950 Hounsfield units at total lung capacity of 7.46%vs4.61%; P= .029). In non-ICS-treated GOLD group D COPD, people with BEC≤100 had more baseline emphysema, prospective exacerbations, and lung function decline. Our analysis has identified a particularly vulnerable subpopulation of people with COPD, suggesting the need for studies focused specifically on their therapeutic treatment. ClinicalTrials.gov; No.: NCT01969344; URL: www. gov.

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