Faculty of Medicine, University of Southampton, Southampton; NIHR Southampton Biomedical Research Centre, University Hospital Southampton, Southampton.
Faculty of Medicine, University of Southampton, Southampton; NIHR Southampton Biomedical Research Centre, University Hospital Southampton, Southampton; Clinical Development, Research and Early Development, Respiratory & Immunology, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden.
Chest. 2021 Apr;159(4):1391-1399. doi: 10.1016/j.chest.2020.11.018. Epub 2020 Nov 25.
Small airways disease (SAD) is a key component of COPD and is a main contributing factor to lung function decline.
Is SAD a key feature of frequent COPD exacerbators and is this related to airway inflammation?
Thirty-nine COPD patients defined as either frequent exacerbator (FE) group (≥ 2 exacerbations/y; n = 17) and infrequent exacerbator (IFE) group (≤ 1 exacerbation/y; n = 22) underwent the forced oscillation technique (resistance at 5 Hz minus 19 Hz [R5-R19], area of reactance [AX]), multiple breath nitrogen washout (conducting airways ventilation heterogeneity, acinar ventilation heterogeneity [S]), plethysmography (ratio of residual volume to total lung capacity), single-breath transfer factor of the lung for carbon monoxide, spirometry (FEV, FEV/FVC), and paired inspiratory-expiratory CT scans to ascertain SAD. A subpopulation underwent bronchoscopy to enable enumeration of BAL cell proportions.
S was significantly higher in the COPD FE group compared with the IFE group (P = .027). In the FE group, markers of SAD were associated strongly with BAL neutrophil proportions, R5-R19 (P = .001, r = 0.795), AX (P = .049, ρ = 0.560), residual volume to total lung capacity ratio (P = .004, r = 0.730), and the mean lung density of the paired CT scans (P = .018, r = 0.639).
Increased S may be a consequence of previous exacerbations or may highlight a group of patients prone to exacerbations. Measures of SAD were associated strongly with neutrophilic inflammation in the small airways of FE patients, supporting the hypothesis that frequent exacerbations are associated with SAD related to increased cellular inflammation.
小气道疾病（SAD）是 COPD 的一个关键组成部分，也是肺功能下降的主要因素。
SAD 是否是 COPD 频繁加重者的一个主要特征，这与气道炎症有关吗？
39 例 COPD 患者被定义为频繁加重者（FE 组，≥ 2 次/年；n = 17）和非频繁加重者（IFE 组，≤ 1 次/年；n = 22），进行强迫振荡技术（5 Hz 与 19 Hz 之间的阻力[R5-R19]、电抗面积[AX]）、多呼吸氮清除（传导气道通气异质性、腺泡通气异质性[S]）、体描法（残气量与肺总量比）、一氧化碳的肺单呼吸转移因子、肺活量计（FEV、FEV/FVC）和配对吸气呼气 CT 扫描以确定 SAD。一部分患者接受支气管镜检查以确定 BAL 细胞比例。
FE 组 COPD 患者的 S 明显高于 IFE 组（P =.027）。在 FE 组中，SAD 标志物与 BAL 中性粒细胞比例、R5-R19（P =.001，r = 0.795）、AX（P =.049，ρ = 0.560）、残气量与肺总量比（P =.004，r = 0.730）和配对 CT 扫描的平均肺密度（P =.018，r = 0.639）密切相关。
S 的增加可能是以前加重的结果，也可能突出了一组容易加重的患者。SAD 指标与 FE 患者小气道中的中性粒细胞炎症密切相关，支持频繁加重与与细胞炎症增加相关的 SAD 有关的假说。
