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Type-2 inflammation and lung function decline in chronic airway disease in the general population
Thorax ( IF 10 ) Pub Date : 2024-04-01 , DOI: 10.1136/thorax-2023-220972
Yunus Çolak , Shoaib Afzal , Jacob Louis Marott , Jørgen Vestbo , Børge Grønne Nordestgaard , Peter Lange

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. Data are available on reasonable request. Additional data regarding technical details, statistical code and derivative data are available from the principal investigator at peter.lange@sund.ku.dk. Data access for further analyses is possible through direct collaborative agreement or through locally managed access arranged through the study’s principal investigator.

中文翻译:

一般人群中慢性气道疾病的 2 型炎症和肺功能下降

背景 目前尚不清楚 2 型炎症是否与哮喘和慢性阻塞性肺病 (COPD) 患者肺功能加速下降有关。我们测试了以下假设:血液嗜酸性粒细胞 (BE) 和呼出一氧化氮 (FeNO) 分数升高表明的 2 型炎症与普通人群肺功能加速下降有关。方法 我们纳入了哥本哈根一般人口研究的成年人,通过后续检查测量了 BE (N=15 605) 和 FeNO (N=2583),并评估了过去 10 年中 1 秒用力呼气量 (FEV1) 的下降情况。根据支气管扩张剂治疗前和治疗后的肺功能、吸烟史和随访检查时的哮喘情况,参与者被分配为无气道疾病、完全可逆性哮喘 (AR)、持续性阻塞性哮喘 (APO)、慢性阻塞性肺病 (COPD) 和非慢性阻塞性肺病 (COPD)。可分类气流限制(NAL)。结果 BE 每升高 100 个细胞/μL,FEV1 下降(以毫升为单位)增加 1.0(95% CI 0.6 至 1.4,p<0.0001);FeNO 每升高 10 ppb,FEV1 下降 3.2(95% CI 2.0 至 4.5,p<0.0001)。BE<300 个细胞/μL 且 FeNO<20 ppb 的患者调整后的 FEV1 下降毫升/年为 18(95% CI 17 至 20),BE≥300 个细胞/μL 或 FeNO≥20 ppb 的患者为 22(19-25) ,以及 27 (21–33) 的 BE≥300 个细胞/μL 和 FeNO≥20 ppb 的患者(趋势 p<0.0001)。AR (0.002) 中相应的 FEV1 下降为 24 (19–29)、33 (25–40) 和 44 (31–56)、26 (14–37)、36 (12–60) 和 56 (24–89) APO 中 (0.07)、COPD 中 32 (27–36)、31 (24–38) 和 44 (24–65) (0.46),以及 COPD 中 27 (21–33)、35 (26–45) 和 37 ( 25-49)在 NAL(0.10)中分别。结论 BE 和 FeNO 升高表明的 2 型炎症与普通人群中慢性气道疾病患者 FEV1 加速下降相关,并且这种关联在哮喘样表型中最为明显。可根据合理要求提供数据。有关技术细节、统计代码和衍生数据的更多数据可从首席研究员处获得,邮箱为 peter.lange@sund.ku.dk。通过直接合作协议或通过研究主要研究者安排的本地管理访问,可以访问用于进一步分析的数据。
更新日期:2024-03-15
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