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A high level of plasma immunoglobulin E (IgE) is associated with an increased risk for severe exacerbation and all-cause mortality in patients with chronic obstructive pulmonary disease (COPD), according to study findings published in the Annals of Allergy, Asthma & Immunology.
Although the blood eosinophil level is a biomarker for predicting the risk for COPD exacerbations, other biomarkers are needed to better identify those patients who would benefit from preventive treatment. Investigators hypothesized that plasma IgE — which is a biomarker for asthma — might also be a potential biomarker for predicting future exacerbation risk in some patients with COPD.
The researchers conducted a study involving 1559 adults with COPD from the Copenhagen General Population Study who had complete information on lung function and plasma IgE concentrations. COPD was defined as having a prebronchodilator forced expiratory volume in 1 second (FEV1)/forced vital capacity of less than 0.70, and FEV1 of less than 80% of predicted in patients aged 40 years and older with chronic respiratory symptoms and smoking exposure of at least 10 pack-years. None of the patients had self-reported asthma.
The probability of severe exacerbation and all-cause mortality was determined with use of the Kaplan-Meier estimator. Severe exacerbations were defined as acute emergency department visits and/or hospital admissions with a primary diagnosis of COPD according to the International Classification of Diseases, 10th Revision. High and low concentrations of plasma IgE were defined by a clinical cutoff of 76 IU/mL.
Among the 1559 patients with COPD, 446 (29%; median age, 66.7 years; 66% male) had plasma IgE of 76 IU/mL or higher. Compared with patients having lesser IgE levels (n=1113; median age, 68.1 years; 52% male), those with IgE of 76 IU/mL or higher had: (1) higher body mass index, tobacco consumption, high-sensitive C-reactive protein levels, and blood eosinophils; (2) greater atopy and cough; and (3) slightly lower lung function measures.
During 14 years of follow-up (median, 6.9; interquartile range, 3.4), 224 severe exacerbations and 434 deaths occurred in the study cohort. Participants with COPD and IgE of 76 IU/mL or greater, compared with those with lesser IgE levels, had a multivariable adjusted hazard ratio (HR) of 1.43 (95% CI, 1.07-1.89) for severe exacerbation and 1.30 (1.05-1.62) for all-cause mortality. When individuals with plasma IgE of 700 IU/mL or greater were excluded, the results were similar, with HRs of 1.44 (1.07-1.93) for severe exacerbation and 1.31 (1.04-1.65) for all-cause mortality.
The researchers also assessed whether IgE levels were linked in any way to the eosinophil levels in patients. In comparison with patients with IgE less than 76 IU/mL and blood eosinophils less than 300 cells/µL, the multivariable adjusted HR for severe exacerbation was 1.12 (0.76-1.67) for those with IgE less than 76 IU/mL and blood eosinophils of 300 cells/µL or greater, 1.62 (1.17-2.24) for IgE of 76 IU/mL or greater and blood eosinophils less than 300 cells/µL, and 1.06 (0.63- 1.77) for those with IgE 76 IU/mL or greater and blood eosinophils of 300 cells/µL or less. The corresponding HRs for all-cause mortality in these 3 groups were 1.27 (0.99-1.63), 1.47 (1.14-1.88), and 1.17 (0.83-1.64), respectively.
No interaction was observed between plasma IgE and blood eosinophils for the risk of severe exacerbation (P for interaction =.11), although a statistically significant negative interaction was found regarding the risk of all-cause mortality (P for interaction =.04).
Potential study limitations include the use of prebronchodilator instead of postbronchodilator spirometric values to diagnose patients with COPD. Because of this, some individuals may have had reversible airflow limitation, which could indicate undiagnosed asthma. Also, only a single measurement of plasma IgE was available, and atopy was based on self-report.
“Our findings suggest that plasma IgE concentration may be a potential prognostic biomarker and treatment target for a subset of COPD patients,” concluded the researchers.
Disclosure: Some of the study authors declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of authors’ disclosures.
Reference
Colak Y, Ingebrigtsen TS, Nordestgaard BG, et al. Plasma immunoglobulin E and risk of exacerbation and mortality in chronic obstructive pulmonary disease: a contemporary population-based cohort. Ann Allergy Asthma Immunol. Published online July 11, 2022. doi:10.1016/j.anai.2022.06.028
This article originally appeared on Pulmonology Advisor
