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一般人群慢性气道疾病中的2型炎症和肺功能下降

2024/06/11

   摘要
   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)患者的肺功能加速下降有关。我们验证了这样一种假设,即在一般人群中,血液嗜酸性粒细胞(BE)和呼出气一氧化氮(FeNO)升高所代表的2型炎症与肺功能加速下降有关。
   方法:我们纳入了哥本哈根总人口研究(Copenhagen General Population Study)中接受过随访检查并测量了BE(15605人)和FeNO(2583人)的成年人,并评估了他们在过去10年中1秒用力呼气容积(FEV1)的下降情况。根据支气管扩张剂使用前后的肺功能、吸烟史和随访检查时的哮喘情况,受试者被分为未患气道疾病、完全可逆性哮喘(AR)、持续阻塞性哮喘(APO)、慢性阻塞性肺疾病(COPD)和无法分类的气流受限(NAL)五组。
   结果:以毫升/年为单位的FEV1下降率为:BE每增加100 cells/μL,FEV1下降率增加1.0(95% CI:0.6-1.4,p<0.0001);FeNO每增加10 ppb,FEV1下降率增加3.2(95% CI:2.0-4.5,p<0.0001)。以毫升/年为单位,调整后的FEV1下降率在BE<300 cells/μL和FeNO< 20 ppb的人群中为18(95% CI:17-20),在 BE≥ 300 cells/μL或FeNO≥ 20 ppb的人群中为22(19-25),在BE≥ 300 cells/μL和FeNO≥ 20 ppb的人群中为27(21-33)(p<0.0001)。相应的FEV1下降分别为:AR组24(19-29)、33(25-40)和44(31-56)(p for trend= 0.002);APO组26(14-37)、36(12-60)和56(24-89)(p for trend= 0.07);COPD组32(27-36)、31(24-38)和44(24-65)(p for trend= 0.46);NAL组27(21-33)、35(26-45)和37(25-49)(p for trend= 0.10)。
   结论:BE和FeNO升高所代表的2型炎症与一般人群中慢性气道疾病患者的FEV1加速下降有关,这种关联在哮喘样表型中最为明显。

 
(四川大学华西医院呼吸与危重症医学科 黄彦立1 王霁1 王刚1译)
(Thorax. 2024 Mar 15;79(4):349-358. doi: 10.1136/thorax-2023-220972. PMID: 38195642; PMCID: PMC10958305.)

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

Çolak Y, Afzal S, Marott JL, Vestbo J, Nordestgaard BG, Lange P.
Thorax. 2024 Mar 15;79(4):349-358. doi: 10.1136/thorax-2023-220972. PMID: 38195642; PMCID: PMC10958305.
 
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 FEV1decline 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.
 



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