Association Between Interstitial Lung Abnormalities and All-Cause Mortality.
Association Between Interstitial Lung Abnormalities and All-Cause Mortality.
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DOI：
10.1001/jama.2016.0518
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发表时间：
2016-02-16
期刊：
影响因子：
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通讯作者：
COPDGene Investigators
中科院分区：
文献类型：
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作者：
Putman RK;Hatabu H;Araki T;Gudmundsson G;Gao W;Nishino M;Okajima Y;Dupuis J;Latourelle JC;Cho MH;El-Chemaly S;Coxson HO;Celli BR;Fernandez IE;Zazueta OE;Ross JC;Harmouche R;Estépar RS;Diaz AA;Sigurdsson S;Gudmundsson EF;Eiríksdottír G;Aspelund T;Budoff MJ;Kinney GL;Hokanson JE;Williams MC;Murchison JT;MacNee W;Hoffmann U;O'Donnell CJ;Launer LJ;Harrris TB;Gudnason V;Silverman EK;O'Connor GT;Washko GR;Rosas IO;Hunninghake GM;Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints (ECLIPSE) Investigators;COPDGene Investigators
肺间质性异常与6分钟步行距离、一氧化碳扩散能力和总肺活量减少有关；然而，据我们所知，与死亡率的关系以前没有调查过。探讨肺间质性异常是否与死亡率增加有关。前瞻性队列研究：2633名参与者来自弗雷明汉心脏研究（FHS） （CT扫描获得9/08 / 3/11），5320名参与者来自年龄基因/环境易感性(AGES)-雷克雅那（招募时间：1/02-2/06），2068名参与者来自COPDGene（招募时间：11/07-4/10），1670名参与者来自COPD纵向评估以确定预测替代终点（ECLIPSE）（招募时间：12/05-12/06）。胸部CT检查确定肺间质性异常。全因死亡率中位随访时间约为3至9年。在AGES-Reykjavik队列中也检查了死因信息。来自FHS的参与者中有177人（7%）出现肺间质性异常，来自AGES-Reykjavik的参与者中有378人（7%），来自COPDGene的参与者中有156人（8%），来自ECLIPSE的参与者中有157人（9%）。在3-9年的中位随访时间内，每个队列中有间质性肺异常的患者比无间质性肺异常的患者死亡更多（绝对死亡率更高）；FHS组为7%比1%（差异6%，95%可信区间[CI] 2%， 10%）， AGES-Reykjavik组为56%比33%（差异23%，95% CI 18%, 28%）， COPDGene组为16%比11%（差异5%，95% CI - 1%, 11%）， ECLIPSE组为11%比11%（差异6%，95% CI 1%, 11%）。校正协变量后，肺间质性异常与FHS队列（HR=2.7, 95% CI, 1.1 - 65， P=0.030）、ags - reykjavik队列（HR 1.3, 95% CI 1.2-1.4， P<0.001）、COPDGene队列（HR=1.8, 95% CI, 1.1, 2.8， P=0.014）和ECLIPSE队列（HR=1.4, 95% CI, 1.1 - 2， P=0.022）的死亡风险增加相关。在AGES-Reykjavik队列中，较高的死亡率可以解释为呼吸系统疾病（特别是肺纤维化）导致的死亡率较高。在四个独立的研究队列中，间质性肺异常与全因死亡率较高的风险相关。这种关联的临床意义需要进一步研究。
Interstitial lung abnormalities have been associated with decreased six-minute walk distance, diffusion capacity for carbon monoxide and total lung capacity; however to our knowledge, an association with mortality has not been previously investigated. To investigate whether interstitial lung abnormalities are associated with increased mortality. Prospective cohort studies of 2633 participants from the Framingham Heart Study (FHS) (CT scans obtained 9/08–3/11), 5320 from the Age Gene/Environment Susceptibility (AGES)-Reykjavik (recruited 1/02–2/06), 2068 from COPDGene (recruited 11/07–4/10), and 1670 from the Evaluation of COPD Longitudinally to Identify Predictive Surrogate End-points (ECLIPSE) (between 12/05–12/06). Interstitial lung abnormality status as determined by chest CT evaluation. All cause mortality over approximately 3 to 9 year median follow up time. Cause-of-death information was also examined in the AGES-Reykjavik cohort. Interstitial lung abnormalities were present in 177 (7%) of the participants from FHS, 378 (7%) from AGES-Reykjavik, 156 (8%) from COPDGene, and in 157 (9%) from ECLIPSE. Over median follow-up times of ~3–9 years there were more deaths (and a greater absolute rate of mortality) among those with interstitial lung abnormalities compared to those without interstitial lung abnormalities in each cohort; 7% compared to 1% in FHS (6% difference, 95% confidence interval [CI] 2%, 10%), 56% compared to 33% in AGES-Reykjavik (23% difference, 95% CI 18%, 28%), 16% compared to 11% in COPDGene (5% difference, 95% CI −1%, 11%) and 11% compared to 5% in ECLIPSE (6% difference, 95% CI 1%, 11%). After adjustment for covariates, interstitial lung abnormalities were associated with an increase in the risk of death in the FHS (HR=2.7, 95% CI, 1.1–65, P=0.030), AGES-Reykjavik (HR 1.3, 95% CI 1.2–1.4, P<0.001), COPDGene (HR=1.8, 95% CI, 1.1, 2.8, P=0.014), and ECLIPSE (HR=1.4, 95% CI, 1.1–2, P=0.022) cohorts. In the AGES-Reykjavik cohort the higher rate of mortality could be explained by a higher rate of death due to respiratory disease, specifically pulmonary fibrosis. In four separate research cohorts, interstitial lung abnormalities were associated with a higher risk of all-cause mortality. The clinical implications of this association require further investigation.