The presence and progression of emphysema in COPD as determined by CT scanning and biomarker expression: a prospective analysis from the ECLIPSE study

The presence and progression of emphysema in COPD as determined by CT scanning and biomarker expression: a prospective analysis from the ECLIPSE study
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DOI:
10.1016/s2213-2600(13)70006-7
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发表时间:
2013-04-01
影响因子:
76.2
通讯作者:
Vestbo, Jorgen
Vestbo, Jorgen
中科院分区:
医学1区
文献类型:
--
作者:
Coxson, Harvey O.;Dirksen, Asger;Vestbo, Jorgen

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背景肺气肿是慢性阻塞性肺疾病(COPD)气流受限的一个关键因素,可以通过CT扫描进行量化。我们研究了一个纵向的国际COPD患者队列的CT肺密度变化。我们还探讨了肺气肿和患者的特征之间的潜在关系,并调查了某些循环生物标志物与CT肺密度下降相关,方法我们使用随机系数模型来评估预测因素的CT肺密度和其纵向变化超过3年的1928例COPD患者参加了评估COPD纵向确定预测替代终点(ECLIPSE)研究。在CT扫描中测量每个体素的肺密度,并在校正肺体积后表示为分布的最低第15百分位点处的密度。本研究在ClinicalTrials.gov注册,编号NCT 00292552。结果基线时的肺密度受年龄、性别、体重指数、当前吸烟状况和吸烟史以及气流受限严重程度的影响。观察到的肺密度下降是可变的(平均每年下降-1.13 g/L [SE 0.06])。女性的肺密度年下降速度(每年增加-0.41 [SE 0.14] g/L,p=0.003)快于男性,当前吸烟者的肺密度年下降速度(每年增加-0.29 [SE 0.14] g/L,p=0.047)快于既往吸烟者。循环水平的生物标志物表面活性蛋白D(SP-D)和可溶性受体的晚期糖基化终产物(sCRP)与基线肺密度和其下降随时间的推移显着相关。解释这项研究表明,在COPD肺密度下降可以测量,它是可变的,并与吸烟和性别。我们确定了肺气肿存在和进展的潜在生化预测因子。
Background Emphysema is a key contributor to airflow limitation in chronic obstructive pulmonary disease (COPD) and can be quantified using CT scanning. We investigated the change in CT lung density in a longitudinal, international cohort of patients with COPD. We also explored the potential relation between emphysema and patient characteristics, and investigated if certain circulating biomarkers were associated with decline in CT lung density.Methods We used a random coefficient model to assess predictors of both CT lung density and its longitudinal change over 3 years in 1928 patients with COPD enrolled in the Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints (ECLIPSE) study. Lung density was measured for every voxel in the CT scan and after correcting for lung volume was expressed as the density at lowest 15th percentile point of the distribution. This study is registered with ClinicalTrials.gov, number NCT00292552.Findings Lung density at baseline was influenced by age, sex, body-mass index, current smoking status and smoking history, and severity of airflow limitation. The observed decline in lung density was variable (mean decline -1.13 g/L [SE 0.06] per year). The annual decline in lung density was more rapid in women (additional -0.41 [SE 0.14] g/L per year, p=0.003) than men and in current smokers (additional -0.29 [SE 0.14] g/L per year, p=0.047) than in former smokers. Circulating levels of the biomarkers surfactant protein D (SP-D) and soluble receptor for advanced glycation endproduct (sRAGE) were significantly associated with both baseline lung density and its decline over time.Interpretation This study shows that decline in lung density in COPD can be measured, that it is variable, and related to smoking and gender. We identified potential biochemical predictors of the presence and progression of emphysema.