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.