Immunoglobulin E (IgE) may be used as a biomarker to help identify individuals with asthma and chronic obstructive pulmonary disease (COPD) overlap (ACO) to differentiate between patients with atopic ACO and patients with nonatopic ACO.

Researchers evaluated a group of patients from the observational COPD Genetic Epidemiology (COPDGene®) study (ClinicalTrials.gov Identifier: NCT00608764),2 which was conducted at 21 clinical centers across the United States. Results of the current study were published in Chronic Obstructive Pulmonary Diseases.1

The researchers used plasma samples from 2870 patients in the COPDGene study to measure total IgE levels and specific IgE levels to 6 common allergens. Patients were divided into 4 groups, which were defined by the presence or absence of COPD (ie, forced expiratory volume in 1 second [FEV1]/forced vital capacity [FVC] <0.7 and FEV1 <80% predicted, corresponding to Global Initiative for Chronic Obstructive Lung Disease [GOLD] spirometry grades 2 to 4)3 and self-reported asthma: (1) asthma, (2) COPD, (3) ACO, and (4) the control group. The control individuals had normal spirometry (ie, FEV1/FVC ≥0.7 and FEV1 ≥80% predicted) and no asthma history.

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Patients with ACO (based on self-reports of asthma) compared with patients with usual COPD exhibited higher total IgE levels (median, 67.0 IU/mL vs 42.2 IU/mL, respectively) and more often had ≥1 positive specific IgE (43.5% vs 24.5%, respectively). The investigators previously used a strict definition of ACO in study patients with COPD based on self-reports of a physician’s diagnosis of asthma at aged <40 years. In this study, the new definition of ACO used was refined by the presence of atopy as established by a total IgE level of >100 IU/mL or ≥1 positive specific IgE. The broader definition of ACO used was based on a self-reported history of asthma.

Patients with all 3 ACO definitions were younger (mean age, 60.0-61.3 years), more often black (36.8%-44.2%), had more airway wall thickening on quantitative analysis of chest computed tomography (CT) scans, and had a higher frequency of exacerbations (1.0-1.2 in the prior year). Of patients with ACO, 37% to 46% did not have atopy. In these individuals, higher rates of emphysema were detected on chest CT scans.

The investigators concluded that according to the associations with exacerbations and CT airway disease observed in this study, the presence of IgE did not clearly enhance the clinical definition of ACO. IgE measurements, however, could be used to distinguish between individuals with atopic ACO and nonatopic ACO who may possess different biologic mechanisms and thus might benefit from potential treatments.

Additional studies are warranted to determine the overlap between atopic ACO and eosinophilic COPD and whether testing for IgE should be used as part of the assessment and management of patients with COPD.

Disclosure: Several study authors declared affiliations with the pharmaceutical industry. Please see the original reference for a full list of authors’ disclosures.

References

1. Hersh CP, Zacharia S, Prakash et al; for the COPDGene® Investigators. Immunoglobulin E as a biomarker for the overlap of atopic asthma and chronic obstructive pulmonary disease. Chronic Obstr Pulm Dis. 2020;7(1):1-12.

2.Regan EA, Hokanson JE, Murphy JR, et al; for the COPDGene® Investigators Genetic epidemiology of COPD (COPDGene) study design. COPD. 2010;7(1):32-43.

3. Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global strategy for the diagnosis, management and prevention of COPD: 2019 Report. https://goldcopd.org/gold-reports/. Published 2019. Accessed February 21, 2020.