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Putman, R.K.* ; Hatabu, H.* ; Araki, T.* ; Gudmundsson, G.* ; Gao, W.* ; Nishino, M.* ; Okajima, Y.* ; Dupuis, J.* ; Latourelle, J.C.* ; Cho, M.H.* ; El-Chemaly, S.* ; Coxson, H.O.* ; Celli, B.R.* ; Fernandez, I.E. ; Zazueta, O.E.* ; Ross, J.C.* ; Harmouche, R.* ; Estépar, R.S.* ; Diaz, A.A.* ; Sigurdsson, S.* ; Gudmundsson, E.F.* ; Eiriksdottir, G.* ; Aspelund, T.* ; Budoff, M.J.* ; Kinney, G.L.* ; Hokanson, J.E.* ; Williams, M.C.* ; Murchison, J.T.* ; MacNee, W.* ; Hoffmann, U.* ; O'Donnell, C.J.* ; Launer, L.J.* ; Harrris, T.B.* ; Gudnason, V.* ; Silverman, E.K.* ; O'Connor, G.T.* ; Washko, G.R.* ; Rosas, I.O.* ; Hunninghake, G.M.*

Association between interstitial lung abnormalities and all-cause mortality.

JAMA 315, 672-681 (2016)
Verlagsversion DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
IMPORTANCE: Interstitial lung abnormalities have been associated with lower 6-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. OBJECTIVE: To investigate whether interstitial lung abnormalities are associated with increased mortality. DESIGN, SETTING, AND POPULATION: Prospective cohort studies of 2633 participants from the FHS (Framingham Heart Study; computed tomographic [CT] scans obtained September 2008-March 2011), 5320 from the AGES-Reykjavik Study (Age Gene/Environment Susceptibility; recruited January 2002-February 2006), 2068 from the COPDGene Study (Chronic Obstructive Pulmonary Disease; recruited November 2007-April 2010), and 1670 from ECLIPSE (Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints; between December 2005-December 2006). EXPOSURES: Interstitial lung abnormality status as determined by chest CT evaluation. MAIN OUTCOMES AND MEASURES: All-cause mortality over an approximate 3- to 9-year median follow-up time. Cause-of-death information was also examined in the AGES-Reykjavik cohort. RESULTS: Interstitial lung abnormalities were present in 177 (7%) of the 2633 participants from FHS, 378 (7%) of 5320 from AGES-Reykjavik, 156 (8%) of 2068 from COPDGene, and in 157 (9%) of 1670 from ECLIPSE. Over median follow-up times of approximately 3 to 9 years, there were more deaths (and a greater absolute rate of mortality) among participants with interstitial lung abnormalities when compared with those who did not have interstitial lung abnormalities in the following cohorts: 7% vs 1% in FHS (6% difference [95% CI, 2% to 10%]), 56% vs 33% in AGES-Reykjavik (23% difference [95% CI, 18% to 28%]), and 11% vs 5% in ECLIPSE (6% difference [95% CI, 1% to 11%]). After adjustment for covariates, interstitial lung abnormalities were associated with a higher risk of death in the FHS (hazard ratio [HR], 2.7 [95% CI, 1.1 to 6.5]; P = .03), AGES-Reykjavik (HR, 1.3 [95% CI, 1.2 to 1.4]; P < .001), COPDGene (HR, 1.8 [95% CI, 1.1 to 2.8]; P = .01), and ECLIPSE (HR, 1.4 [95% CI, 1.1 to 2.0]; P = .02) 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. CONCLUSIONS AND RELEVANCE: In 4 separate research cohorts, interstitial lung abnormalities were associated with a greater risk of all-cause mortality. The clinical implications of this association require further investigation.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Idiopathic Pulmonary-fibrosis; Muc5b Promoter Polymorphism; Exercise Capacity; Disease; Susceptibility; Epidemiology; Prevalence
ISSN (print) / ISBN 0098-7484
e-ISSN 1538-3598
Zeitschrift JAMA: Journal of the American Medical Association
Quellenangaben Band: 315, Heft: 7, Seiten: 672-681 Artikelnummer: , Supplement: ,
Verlag American Medical Association
Verlagsort Chicago
Begutachtungsstatus