Plasma immunoglobulin E and risk of exacerbation and mortality in chronic obstructive pulmonary disease: A contemporary population-based cohort
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Plasma immunoglobulin E and risk of exacerbation and mortality in chronic obstructive pulmonary disease : A contemporary population-based cohort. / Çolak, Yunus; Sylvan Ingebrigtsen, Truls; Nordestgaard, Børge G.; Marott, Jacob L.; Lange, Peter; Vestbo, Jørgen; Afzal, Shoaib.
I: Annals of Allergy, Asthma and Immunology, Bind 129, Nr. 4, 2022, s. 490-496.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Plasma immunoglobulin E and risk of exacerbation and mortality in chronic obstructive pulmonary disease
T2 - A contemporary population-based cohort
AU - Çolak, Yunus
AU - Sylvan Ingebrigtsen, Truls
AU - Nordestgaard, Børge G.
AU - Marott, Jacob L.
AU - Lange, Peter
AU - Vestbo, Jørgen
AU - Afzal, Shoaib
N1 - Funding Information: Disclosures: Dr Çolak reports personal fees from Boehringer-Ingelheim, AstraZeneca, and Sanofi Genzyme. Dr Ingebrigtsen has received fee for speaking from AstraZeneca, not related to the topic of this study. Dr Lange reports grants and personal fees from Almirall, GlaxoSmithKline, and Boehringer-Ingelheim and personal fees from AstraZeneca, Novartis, Nycomed, Pfizer, and Mundipharma outside the submitted work. Dr Vestbo reports personal fees from Boehringer-Ingelheim, GlaxoSmithKline, Chiesi Pharmaceuticals, Novartis, and AstraZeneca outside the submitted work. The other authors have no conflicts of interest to report. The views expressed are those of the authors. Funding: The Capital Region of Copenhagen, Danish Lung Foundation, Velux Foundation, Copenhagen University Hospital – Herlev and Gentofte, and Lundbeck Foundation. Dr Vestbo is supported by the National Institute for Health and Care Research Manchester Biomedical Research Centre. Funding Information: Funding: The Capital Region of Copenhagen, Danish Lung Foundation, Velux Foundation, Copenhagen University Hospital – Herlev and Gentofte, and Lundbeck Foundation. Dr Vestbo is supported by the National Institute for Health and Care Research Manchester Biomedical Research Centre. Publisher Copyright: © 2022 The Authors
PY - 2022
Y1 - 2022
N2 - Background: Novel biomarkers and targeted treatments are needed for patients with chronic obstructive pulmonary disease (COPD). Objective: To test the hypothesis that high plasma immunoglobulin (Ig)E concentrations associate with increased risk of exacerbation and mortality in individuals with COPD in the general population. Methods: Among 46,598 adults in the Copenhagen General Population Study, we included 1559 with COPD, defined as forced expiratory volume in 1 second/forced vital capacity < 0.70 and forced expiratory volume in 1 second < 80% predicted in individuals aged ≥ 40 years with chronic respiratory symptoms and smoking exposure ≥ 10 pack-years, and without asthma. We assessed risk of future severe exacerbation and all-cause mortality according to baseline plasma IgE ≥ 76 IU/mL, a clinical cutoff for omalizumab treatment in severe asthma. Results: During 14 years of follow-up (median, 6.9; interquartile range, 3.4), we recorded 224 severe exacerbations and 434 deaths in 1559 individuals with COPD. Individuals with COPD with IgE ≥ 76 IU/mL vs those with < 76 IU/mL had a multivariable adjusted hazard ratio (HR) of 1.43 (95% confidence interval, 1.07-1.89) for severe exacerbation and 1.30 (1.05-1.62) for all-cause mortality. Compared with individuals with IgE < 76 IU/mL and blood eosinophils < 300 cells/µL, the multivariable adjusted HR for severe exacerbation was 1.12 (0.76-1.67) for those with IgE < 76 IU/mL and blood eosinophils ≥ 300 cells/µL, 1.62 (1.17-2.24) for IgE ≥ 76 IU/mL and blood eosinophils < 300 cells/µL, and 1.06 (0.63-1.77) for those with IgE ≥ 76 IU/mL and blood eosinophils ≥ 300 cells/µL. Corresponding HRs for all-cause mortality were 1.27 (0.99-1.63), 1.47 (1.14-1.88), and 1.17 (0.83-1.64), respectively. Conclusion: High plasma IgE was associated with an increased risk of severe exacerbation and all-cause mortality in individuals with COPD in the general population, independent of blood eosinophils.
AB - Background: Novel biomarkers and targeted treatments are needed for patients with chronic obstructive pulmonary disease (COPD). Objective: To test the hypothesis that high plasma immunoglobulin (Ig)E concentrations associate with increased risk of exacerbation and mortality in individuals with COPD in the general population. Methods: Among 46,598 adults in the Copenhagen General Population Study, we included 1559 with COPD, defined as forced expiratory volume in 1 second/forced vital capacity < 0.70 and forced expiratory volume in 1 second < 80% predicted in individuals aged ≥ 40 years with chronic respiratory symptoms and smoking exposure ≥ 10 pack-years, and without asthma. We assessed risk of future severe exacerbation and all-cause mortality according to baseline plasma IgE ≥ 76 IU/mL, a clinical cutoff for omalizumab treatment in severe asthma. Results: During 14 years of follow-up (median, 6.9; interquartile range, 3.4), we recorded 224 severe exacerbations and 434 deaths in 1559 individuals with COPD. Individuals with COPD with IgE ≥ 76 IU/mL vs those with < 76 IU/mL had a multivariable adjusted hazard ratio (HR) of 1.43 (95% confidence interval, 1.07-1.89) for severe exacerbation and 1.30 (1.05-1.62) for all-cause mortality. Compared with individuals with IgE < 76 IU/mL and blood eosinophils < 300 cells/µL, the multivariable adjusted HR for severe exacerbation was 1.12 (0.76-1.67) for those with IgE < 76 IU/mL and blood eosinophils ≥ 300 cells/µL, 1.62 (1.17-2.24) for IgE ≥ 76 IU/mL and blood eosinophils < 300 cells/µL, and 1.06 (0.63-1.77) for those with IgE ≥ 76 IU/mL and blood eosinophils ≥ 300 cells/µL. Corresponding HRs for all-cause mortality were 1.27 (0.99-1.63), 1.47 (1.14-1.88), and 1.17 (0.83-1.64), respectively. Conclusion: High plasma IgE was associated with an increased risk of severe exacerbation and all-cause mortality in individuals with COPD in the general population, independent of blood eosinophils.
U2 - 10.1016/j.anai.2022.06.028
DO - 10.1016/j.anai.2022.06.028
M3 - Journal article
C2 - 35835293
AN - SCOPUS:85135497970
VL - 129
SP - 490
EP - 496
JO - Annals of Allergy, Asthma, & Immunology
JF - Annals of Allergy, Asthma, & Immunology
SN - 1081-1206
IS - 4
ER -
ID: 322488009