Department of Radiology, University of British Columbia, Vancouver, Canada.
Gentofte Hospital, University of Copenhagen, Hellerup, Denmark.
Lancet Respir Med. 2013 Apr;1(2):129-36. doi: 10.1016/S2213-2600(13)70006-7. Epub 2013 Feb 1.
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.
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.
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.
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.
GlaxoSmithKline.
肺气肿是慢性阻塞性肺疾病（COPD）气流受限的主要原因，可以通过 CT 扫描进行量化。我们调查了 COPD 患者的 CT 肺密度在纵向国际队列中的变化。我们还探讨了肺气肿与患者特征之间的潜在关系，并研究了某些循环生物标志物是否与 CT 肺密度下降有关。
我们使用随机系数模型评估了 1928 名 COPD 患者的 CT 肺密度及其在 3 年内的纵向变化的预测因子，这些患者参加了 COPD 的评估以确定预测替代终点（ECLIPSE）研究。在 CT 扫描中对每个体素进行了肺密度测量，并且在对肺容积进行校正后，将其表示为分布的最低 15%分位数点的密度。该研究在 ClinicalTrials.gov 上注册，编号为 NCT00292552。
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（每年下降-1.13 g/L[SE 0.06]）。女性的肺密度每年下降更快（每年增加-0.41[SE 0.14]g/L，p=0.003），而男性和以前的吸烟者则更快（每年增加-0.29[SE 0.14]g/L，p=0.047）。生物标志物表面活性剂蛋白 D（SP-D）和可溶性晚期糖基化终产物受体（sRAGE）的循环水平与基线时的肺密度及其随时间的下降均显著相关。
这项研究表明，COPD 中肺密度的下降可以被测量，其变化与吸烟和性别有关。我们确定了肺气肿存在和进展的潜在生化预测因子。
葛兰素史克公司。
