Airway wall thickening on CT: Relation to smoking status and severity of COPD
Airway wall thickening on CT: Relation to smoking status and severity of COPD
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DOI：
10.1016/j.rmed.2018.11.014
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发表时间：
2019-01-01
影响因子：
4.3
通讯作者：
Lynch, David A.
中科院分区：
文献类型：
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作者：
Charbonnier, Jean-Paul;Pompe, Esther;Lynch, David A.
吸烟者的气道壁增厚被认为是炎症变化和气道重塑的结果。这项研究调查了是否CT衍生的气道壁增厚与疾病的严重程度在吸烟者和无COPD，如果气道壁增厚是可逆的戒烟。我们检查了2000名吸烟者和46名从不吸烟者谁返回的5年随访访问的COPDGene研究。在第1次访视时进行多变量回归分析，以将气道壁厚度（表示为Pi 10）与1秒用力呼气量预测百分比（FEV1%预测值）、6分钟步行距离（6 MWD）和圣乔治呼吸问卷（SGRQ）相关联。采用线性混合模型进行纵向分析，评估戒烟对Pi 10的影响，Pi 10越高，所有GOLD分期中FEV1%预测值、6 MWD和SGRQ越差。纵向分析显示，戒烟的受试者的Pi 10显著降低（Δ Pi 10 = -0.18 mm，p < 0.001）。开始吸烟的受试者的Pi 10显著增加（Δ Pi 10 = 0.14 mm，p < 0.001）。Pi 10是吸烟者伴和不伴COPD的吸烟相关气道损伤的临床相关生物标志物。随着吸烟状态的变化，Pi 10的变化表明它可以量化吸烟相关气道炎症的可逆成分。
Airway wall thickening in cigarette smokers is thought to be a result of inflammatory changes and airway remodeling. This study investigates if CT-derived airway wall thickening associates to disease severity in smokers with and without COPD and if airway wall thickening is reversible by smoking cessation.We examined 2000 smokers and 46 never-smokers who returned for a 5-year follow-up visit in the COPDGene-study. Multivariable regression analyses were performed at visit 1 to associate airway wall thickness (expressed as Pi10) with percent predicted forced expiratory volume in 1 s (FEV1%-predicted), 6-min walking distance (6MWD), and St. George Respiratory Questionnaire (SGRQ). Longitudinal analyses were performed to assess the effect of smoking cessation on Pi10 using linear mixed models.A higher Pi10 was significantly associated with worse FEV1%-predicted, 6MWD, and SGRQ in all GOLD-stages. Longitudinal analyses showed that subjects that quit smoking significantly decreased in Pi10 (Delta Pi10 = -0.18 mm, p < 0.001). Subjects that started smoking had a significant increase in Pi10 (Delta Pi10 = 0.14 mm, p < 0.001).Pi10 is a clinically relevant biomarker of smoking-related airway injury in smokers with and without COPD. The change in Pi10 with change in smoking status suggests that it can quantify a reversible component of smoking-related airway inflammation.