Type-2 inflammation and lung function decline in chronic airway disease in the general population

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Type-2 inflammation and lung function decline in chronic airway disease in the general population. / Çolak, Yunus; Afzal, Shoaib; Marott, Jacob Louis; Vestbo, Jørgen; Nordestgaard, Børge Grønne; Lange, Peter.

I: Thorax, Bind 79, Nr. 4, 2024.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Çolak, Y, Afzal, S, Marott, JL, Vestbo, J, Nordestgaard, BG & Lange, P 2024, 'Type-2 inflammation and lung function decline in chronic airway disease in the general population', Thorax, bind 79, nr. 4. https://doi.org/10.1136/thorax-2023-220972

APA

Çolak, Y., Afzal, S., Marott, J. L., Vestbo, J., Nordestgaard, B. G., & Lange, P. (2024). Type-2 inflammation and lung function decline in chronic airway disease in the general population. Thorax, 79(4). https://doi.org/10.1136/thorax-2023-220972

Vancouver

Çolak Y, Afzal S, Marott JL, Vestbo J, Nordestgaard BG, Lange P. Type-2 inflammation and lung function decline in chronic airway disease in the general population. Thorax. 2024;79(4). https://doi.org/10.1136/thorax-2023-220972

Author

Çolak, Yunus ; Afzal, Shoaib ; Marott, Jacob Louis ; Vestbo, Jørgen ; Nordestgaard, Børge Grønne ; Lange, Peter. / Type-2 inflammation and lung function decline in chronic airway disease in the general population. I: Thorax. 2024 ; Bind 79, Nr. 4.

Bibtex

@article{2d1c3569ec10440981fd854eafffb5ef,
title = "Type-2 inflammation and lung function decline in chronic airway disease in the general population",
abstract = "BACKGROUND: It is unclear if type-2 inflammation is associated with accelerated lung function decline in individuals with asthma and chronic obstructive pulmonary disease (COPD). We tested the hypothesis that type-2 inflammation indicated by elevated blood eosinophils (BE) and fraction of exhaled nitric oxide (FeNO) is associated with accelerated lung function decline in the general population.METHODS: We included adults from the Copenhagen General Population Study with measurements of BE (N=15 605) and FeNO (N=2583) from a follow-up examination and assessed forced expiratory volume in 1 s (FEV1) decline in the preceding 10 years. Based on pre- and post-bronchodilator lung function, smoking history and asthma at follow-up examination, participants were assigned as not having airway disease, asthma with full reversibility (AR), asthma with persistent obstruction (APO), COPD, and not classifiable airflow limitation (NAL).RESULTS: FEV1 decline in mL/year increased with 1.0 (95% CI 0.6 to 1.4, p<0.0001) per 100 cells/µL higher BE and with 3.2 (95% CI 2.0 to 4.5, p<0.0001) per 10 ppb higher FeNO. Adjusted FEV1 decline in mL/year was 18 (95% CI 17 to 20) in those with BE<300 cells/µL and FeNO<20 ppb, 22 (19-25) in BE≥300 cells/µL or FeNO≥20 ppb, and 27 (21-33) in those with BE≥300 cells/µL and FeNO≥20 ppb (p for trend<0.0001). Corresponding FEV1 declines were 24 (19-29), 33 (25-40) and 44 (31-56) in AR (0.002), 26 (14-37), 36 (12-60) and 56 (24-89) in APO (0.07), 32 (27-36), 31 (24-38) and 44 (24-65) in COPD (0.46), and 27 (21-33), 35 (26-45), and 37 (25-49) in NAL (0.10), respectively.CONCLUSIONS: Type-2 inflammation indicated by elevated BE and FeNO is associated with accelerated FEV1 decline in individuals with chronic airway disease in the general population, and this association was most pronounced in an asthma-like phenotype.",
author = "Yunus {\c C}olak and Shoaib Afzal and Marott, {Jacob Louis} and J{\o}rgen Vestbo and Nordestgaard, {B{\o}rge Gr{\o}nne} and Peter Lange",
note = "{\textcopyright} Author(s) (or their employer(s)) 2024. No commercial re-use. See rights and permissions. Published by BMJ.",
year = "2024",
doi = "10.1136/thorax-2023-220972",
language = "English",
volume = "79",
journal = "Thorax",
issn = "0040-6376",
publisher = "B M J Group",
number = "4",

}

RIS

TY - JOUR

T1 - Type-2 inflammation and lung function decline in chronic airway disease in the general population

AU - Çolak, Yunus

AU - Afzal, Shoaib

AU - Marott, Jacob Louis

AU - Vestbo, Jørgen

AU - Nordestgaard, Børge Grønne

AU - Lange, Peter

N1 - © Author(s) (or their employer(s)) 2024. No commercial re-use. See rights and permissions. Published by BMJ.

PY - 2024

Y1 - 2024

N2 - BACKGROUND: It is unclear if type-2 inflammation is associated with accelerated lung function decline in individuals with asthma and chronic obstructive pulmonary disease (COPD). We tested the hypothesis that type-2 inflammation indicated by elevated blood eosinophils (BE) and fraction of exhaled nitric oxide (FeNO) is associated with accelerated lung function decline in the general population.METHODS: We included adults from the Copenhagen General Population Study with measurements of BE (N=15 605) and FeNO (N=2583) from a follow-up examination and assessed forced expiratory volume in 1 s (FEV1) decline in the preceding 10 years. Based on pre- and post-bronchodilator lung function, smoking history and asthma at follow-up examination, participants were assigned as not having airway disease, asthma with full reversibility (AR), asthma with persistent obstruction (APO), COPD, and not classifiable airflow limitation (NAL).RESULTS: FEV1 decline in mL/year increased with 1.0 (95% CI 0.6 to 1.4, p<0.0001) per 100 cells/µL higher BE and with 3.2 (95% CI 2.0 to 4.5, p<0.0001) per 10 ppb higher FeNO. Adjusted FEV1 decline in mL/year was 18 (95% CI 17 to 20) in those with BE<300 cells/µL and FeNO<20 ppb, 22 (19-25) in BE≥300 cells/µL or FeNO≥20 ppb, and 27 (21-33) in those with BE≥300 cells/µL and FeNO≥20 ppb (p for trend<0.0001). Corresponding FEV1 declines were 24 (19-29), 33 (25-40) and 44 (31-56) in AR (0.002), 26 (14-37), 36 (12-60) and 56 (24-89) in APO (0.07), 32 (27-36), 31 (24-38) and 44 (24-65) in COPD (0.46), and 27 (21-33), 35 (26-45), and 37 (25-49) in NAL (0.10), respectively.CONCLUSIONS: Type-2 inflammation indicated by elevated BE and FeNO is associated with accelerated FEV1 decline in individuals with chronic airway disease in the general population, and this association was most pronounced in an asthma-like phenotype.

AB - BACKGROUND: It is unclear if type-2 inflammation is associated with accelerated lung function decline in individuals with asthma and chronic obstructive pulmonary disease (COPD). We tested the hypothesis that type-2 inflammation indicated by elevated blood eosinophils (BE) and fraction of exhaled nitric oxide (FeNO) is associated with accelerated lung function decline in the general population.METHODS: We included adults from the Copenhagen General Population Study with measurements of BE (N=15 605) and FeNO (N=2583) from a follow-up examination and assessed forced expiratory volume in 1 s (FEV1) decline in the preceding 10 years. Based on pre- and post-bronchodilator lung function, smoking history and asthma at follow-up examination, participants were assigned as not having airway disease, asthma with full reversibility (AR), asthma with persistent obstruction (APO), COPD, and not classifiable airflow limitation (NAL).RESULTS: FEV1 decline in mL/year increased with 1.0 (95% CI 0.6 to 1.4, p<0.0001) per 100 cells/µL higher BE and with 3.2 (95% CI 2.0 to 4.5, p<0.0001) per 10 ppb higher FeNO. Adjusted FEV1 decline in mL/year was 18 (95% CI 17 to 20) in those with BE<300 cells/µL and FeNO<20 ppb, 22 (19-25) in BE≥300 cells/µL or FeNO≥20 ppb, and 27 (21-33) in those with BE≥300 cells/µL and FeNO≥20 ppb (p for trend<0.0001). Corresponding FEV1 declines were 24 (19-29), 33 (25-40) and 44 (31-56) in AR (0.002), 26 (14-37), 36 (12-60) and 56 (24-89) in APO (0.07), 32 (27-36), 31 (24-38) and 44 (24-65) in COPD (0.46), and 27 (21-33), 35 (26-45), and 37 (25-49) in NAL (0.10), respectively.CONCLUSIONS: Type-2 inflammation indicated by elevated BE and FeNO is associated with accelerated FEV1 decline in individuals with chronic airway disease in the general population, and this association was most pronounced in an asthma-like phenotype.

U2 - 10.1136/thorax-2023-220972

DO - 10.1136/thorax-2023-220972

M3 - Journal article

C2 - 38195642

VL - 79

JO - Thorax

JF - Thorax

SN - 0040-6376

IS - 4

ER -

ID: 380287950