Relationship of Blood Eosinophil Count to Exacerbations in Chronic Obstructive Pulmonary Disease

Background: Eosinophilic airway inflammation characterizes a chronic obstructive pulmonary disease (COPD) phenotype that requires more study.

Objective: To investigate the relationship of blood eosinophil count to exacerbations in COPD.

Methods: Using administrative pharmacy and health care utilization data from 2009 to 2012, we retrospectively identified patients 40 years or older with a COPD diagnosis, postbronchodilator FEV₁/forced vital capacity ratio of less than 0.7, and a blood eosinophil count (N = 7,245). COPD exacerbations were defined as hospitalizations or emergency department visits with a primary diagnosis of COPD, or outpatient visits with systemic corticosteroid dispensing within ±14 days associated with an encounter code consistent with a COPD exacerbation. The relationship between the index blood eosinophil count and the rate of COPD exacerbations in the follow-up year was determined by multivariable analyses.

Results: Patients with COPD were predominantly male (57.1%), white (71.8%), often current or past smokers (75.4%), and had frequent comorbidities; 19.0% had eosinophil counts of greater than or equal to 300 cells/mm³, 76.1% were classified as moderate to very severe by lung function, and the COPD exacerbation rate was 0.38 per year (95% CI, 0.37-0.40). After adjustment for potential confounders, COPD exacerbations during 1-year follow-up were significantly greater for patients with blood eosinophil counts of greater than or equal to 300 cells/mm³ (rate ratio [RR], 1.25; 95% CI, 1.10-1.43), greater than or equal to 400 cells/mm³ (RR, 1.48; 95% CI, 1.26-1.75), and greater than or equal to 500 cells/mm³ (RR, 1.76; 95% CI, 1.45-2.14), respectively, compared with patients with eosinophils lower than the cutoffs.

Conclusions: In this study, high blood eosinophil counts were an independent risk factor for future exacerbations in patients with COPD, a phenotype that might benefit from therapy directed at eosinophilic-driven disease and inflammation.