المؤلفون: Pistenmaa, Carrie L, Nardelli, P, Ash, SY, Come, CE, Diaz, AA, Rahaghi, FN, Barr, RG, Young, KA, Kinney, GL, Simmons, JP, Wade, RC, Wells, JM, Hokanson, JE, Washko, GR, San José Estépar, R, Crapo, James D, Silverman, Edwin K, Make, Barry J, Regan, Elizabeth A, Beaty, Terri H, Castaldi, Peter J, Cho, Michael H, DeMeo, Dawn L, Boueiz, Adel El, Foreman, Marilyn G, Ghosh, Auyon, Hayden, Lystra P, Hersh, Craig P, Hetmanski, Jacqueline, Hobbs, Brian D, Hokanson, John E, Kim, Wonji, Laird, Nan, Lange, Christoph, Lutz, Sharon M, McDonald, Merry-Lynn, Prokopenko, Dmitry, Moll, Matthew, Morrow, Jarrett, Qiao, Dandi, Regan, Elizabeth, Saferali, Aabida, Sakornsakolpat, Phuwanat, Wan, Emily S, Yun, Jeong, Centeno, Juan Pablo, Charbonnier, Jean-Paul, Coxson, Harvey O, Galban, Craig J, Han, MeiLan K, Hoffman, Eric A, Humphries, Stephen, Jacobson, Francine L, Judy, Philip F, Kazerooni, Ella A, Kluiber, Alex, Lynch, David A, Nardelli, Pietro, Newell, John D, Notary, Aleena, Oh, Andrea, Ross, James C, San Jose Estepar, Raul, Schroeder, Joyce, Sieren, Jered, Stoel, Berend C, Tschirren, Juerg, Van Beek, Edwin, Ginneken, Bramvan, van Rikxoort, Eva, Ferrero, Gonzalo Vegas Sanchez-, Veitel, Lucas, Washko, George R, Wilson, Carla G, Jensen, Robert, Everett, Douglas, Crooks, Jim, Pratte, Katherine, Strand, Matt, Austin, Erin, Kinney, Gregory, Young, Kendra A, Bhatt, Surya P, Bon, Jessica, Diaz, Alejandro A, Make, Barry, Murray, Susan, Soler, Xavier, Bowler, Russell P, Kechris, Katerina, Banaei-Kashani, Farnoush, Curtis, Jeffrey L

المصدر: CHEST Journal. 160(2)

مصطلحات موضوعية: Emphysema, Tobacco, Tobacco Smoke and Health, Lung, Chronic Obstructive Pulmonary Disease, Clinical Research, Biomedical Imaging, Respiratory, Disease Progression, Endothelium, Vascular, Female, Humans, Longitudinal Studies, Male, Middle Aged, Pulmonary Artery, Pulmonary Disease, Chronic Obstructive, Respiratory Function Tests, Smokers, Tomography, X-Ray Computed, emphysema, imaging, longitudinal, lung function, pulmonary circulation, COPDGene Investigators, Clinical Sciences, Respiratory System

الوصف: BackgroundPulmonary endothelial damage has been shown to precede the development of emphysema in animals, and vascular changes in humans have been observed in COPD and emphysema.Research questionIs intraparenchymal vascular pruning associated with longitudinal progression of emphysema on CT imaging or decline in lung function over 5 years?Study design and methodsThe Genetic Epidemiology of COPD Study enrolled ever smokers with and without COPD from 2008 through 2011. The percentage of emphysema-like lung, or "percent emphysema," was assessed at baseline and after 5 years on noncontrast CT imaging as the percentage of lung voxels < -950 Hounsfield units. An automated CT imaging-based tool assessed and classified intrapulmonary arteries and veins. Spirometry measures are postbronchodilator. Pulmonary arterial pruning was defined as a lower ratio of small artery volume (< 5 mm2 cross-sectional area) to total lung artery volume. Mixed linear models included demographics, anthropomorphics, smoking, and COPD, with emphysema models also adjusting for CT imaging scanner and lung function models adjusting for clinical center and baseline percent emphysema.ResultsAt baseline, the 4,227 participants were 60 ± 9 years of age, 50% were women, 28% were Black, 47% were current smokers, and 41% had COPD. Median percent emphysema was 2.1 (interquartile range, 0.6-6.3) and progressed 0.24 percentage points/y (95% CI, 0.22-0.26 percentage points/y) over 5.6 years. Mean FEV1 to FVC ratio was 68.5 ± 14.2% and declined 0.26%/y (95% CI, -0.30 to -0.23%/y). Greater pulmonary arterial pruning was associated with more rapid progression of percent emphysema (0.11 percentage points/y per 1-SD increase in arterial pruning; 95% CI, 0.09-0.16 percentage points/y), including after adjusting for baseline percent emphysema and FEV1. Arterial pruning also was associated with a faster decline in FEV1 to FVC ratio (-0.04%/y per 1-SD increase in arterial pruning; 95% CI, -0.008 to -0.001%/y).InterpretationPulmonary arterial pruning was associated with faster progression of percent emphysema and more rapid decline in FEV1 to FVC ratio over 5 years in ever smokers, suggesting that pulmonary vascular differences may be relevant in disease progression.Trial registryClinicalTrials.gov; No.: NCT00608764; URL: www.clinicaltrials.gov.

وصف الملف: application/pdf

الوصول الحر: https://escholarship.org/uc/item/0xj6q524Test

المؤلفون: Li Y, Dai R, Gwon Y, Rennard SI, Make BJ, Foer D, Strand MJ, Austin E, Young KA, Hokanson JE, Pratte KA, Conway R, Kinney GL

المصدر: Clinical Epidemiology, Vol Volume 14, Pp 731-735 (2022)

مصطلحات موضوعية: Infectious and parasitic diseases, RC109-216

الوصف: Yisha Li,1 Ran Dai,2 Yeongjin Gwon,2 Stephen I Rennard,3 Barry J Make,4 Dinah Foer,5 Matthew J Strand,4 Erin Austin,6 Kendra A Young,1 John E Hokanson,1 Katherine A Pratte,7 Rebecca Conway,1 Gregory L Kinney1 On behalf of COPDGene investigators1Department of Epidemiology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA; 2Department of Biostatistics, School of Public Health, University of Nebraska Medical Center, Omaha, NE, USA; 3Division of Pulmonary, Critical Care and Sleep Medicine, University of Nebraska Medical Center, Omaha, NE, USA; 4Department of Medicine, National Jewish Health, Denver, CO, USA; 5Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA; 6Mathematical and Statistical Sciences, University of Colorado Denver, Denver, CO, USA; 7Department of Biostatistics, National Jewish Health, Denver, CO, USACorrespondence: Gregory L Kinney, Department of Epidemiology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA, Tel +1 303-724-4437, Email GREG.KINNEY@CUANSCHUTZ.EDU

وصف الملف: electronic resource

العلاقة: https://www.dovepress.com/identifying-individual-medications-affecting-pulmonary-outcomes-when-m-peer-reviewed-fulltext-article-CLEPTest; https://doaj.org/toc/1179-1349Test

الوصول الحر: https://doaj.org/article/197f65e91a4d4292b52324b363ce2589Test

المؤلفون: Kurniansyah, N, Goodman, MO, Khan, AT, Wang, J, Feofanova, E, Bis, JC, Wiggins, KL, Huffman, JE, Kelly, T, Elfassy, T, Guo, X, Palmas, W, Lin, HJ, Hwang, S-J, Gao, Y, Young, K, Kinney, GL, Smith, JA, Yu, B, Liu, S, Wassertheil-Smoller, S, Manson, JE, Zhu, X, Chen, Y-DI, Lee, I-T, Gu, CC, Lloyd-Jones, DM, Zöllner, S, Fornage, M, Kooperberg, C, Correa, A, Psaty, BM, Arnett, DK, Isasi, CR, Rich, SS, Kaplan, RC, Redline, S, Mitchell, BD, Franceschini, N, Levy, D, Rotter, JI, Morrison, AC, Sofer, T

مصطلحات موضوعية: Male, Female, Humans, Blood Pressure, Population Health, Risk Factors, Multifactorial Inheritance, Ethnicity, Genome-Wide Association Study, Genetic Predisposition to Disease

الوصف: We assess performance and limitations of polygenic risk scores (PRSs) for multiple blood pressure (BP) phenotypes in diverse population groups. We compare "clumping-and-thresholding" (PRSice2) and LD-based (LDPred2) methods to construct PRSs from each of multiple GWAS, as well as multi-PRS approaches that sum PRSs with and without weights, including PRS-CSx. We use datasets from the MGB Biobank, TOPMed study, UK biobank, and from All of Us to train, assess, and validate PRSs in groups defined by self-reported race/ethnic background (Asian, Black, Hispanic/Latino, and White). For both SBP and DBP, the PRS-CSx based PRS, constructed as a weighted sum of PRSs developed from multiple independent GWAS, perform best across all race/ethnic backgrounds. Stratified analysis in All of Us shows that PRSs are better predictive of BP in females compared to males, individuals without obesity, and middle-aged (40-60 years) compared to older and younger individuals.

العلاقة: Nature Communications; Kurniansyah, N., Goodman, M.O., Khan, A.T. et al. Evaluating the use of blood pressure polygenic risk scores across race/ethnic background groups. Nat Commun 14, 3202 (2023). https://doi.org/10.1038/s41467-023-38990-9Test; https://qmro.qmul.ac.uk/xmlui/handle/123456789/93324Test

الإتاحة: https://doi.org/10.1038/s41467-023-38990-9Test
https://qmro.qmul.ac.uk/xmlui/handle/123456789/93324Test

المؤلفون: Li Y, Ragland M, Austin E, Young K, Pratte K, Hokanson JE, Beaty TH, Regan EA, Rennard SI, Wern C, Jacobs MR, Tal-Singer R, Make BJ, Kinney GL

المصدر: Clinical Epidemiology, Vol Volume 12, Pp 1171-1181 (2020)

مصطلحات موضوعية: copdgene, co-morbidities, latent class analysis, medication patterns, mortality, Infectious and parasitic diseases, RC109-216

الوصف: Yisha Li,1 Margaret Ragland,1 Erin Austin,2 Kendra Young,1 Katherine Pratte,3 John E Hokanson,1 Terri H Beaty,4 Elizabeth A Regan,3 Stephen I Rennard,5 Christina Wern,6 Michael R Jacobs,7 Ruth Tal-Singer,8 Barry J Make,3 Gregory L Kinney1 On Behalf of theCOPDGene investigators1Department of Epidemiology, Colorado School of Public Health, University of Colorado Anschutz Medical Campus, Aurora, CO, USA; 2Mathematical and Statistical Sciences, University of Colorado Denver, Denver, CO, USA; 3National Jewish Health, Denver, CO, USA; 4Bloomberg School of Public Health, University of John Hopkins, Baltimore, MD, USA; 5Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NB, USA; 6Department of Clinical Pharmacy, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA; 7School of Pharmacy, Temple University, PA, Pennsylvania, USA; 8COPD Foundation, Washington, D.C., USACorrespondence: Gregory L KinneyDepartment of Epidemiology, Colorado School of Public Health, University of Colorado Anschutz Medical Campus, Aurora, CO, USATel +1 303-724-4437Email GREG.KINNEY@CUANSCHUTZ.EDUPurpose: Medication patterns include all medications in an individual’s clinical profile. We aimed to identify chronic co-morbidity treatment patterns through medication use among COPDGene participants and determine whether these patterns were associated with mortality, acute exacerbations of chronic obstructive pulmonary disease (AECOPD) and quality of life.Materials and Methods: Participants analyzed here completed Phase 1 (P1) and/or Phase 2 (P2) of COPDGene. Latent class analysis (LCA) was used to identify medication patterns and assign individuals into unobserved LCA classes. Mortality, AECOPD, and the St. George’s Respiratory Questionnaire (SGRQ) health status were compared in different LCA classes through survival analysis, logistic regression, and Kruskal–Wallis test, respectively.Results: LCA identified 8 medication patterns from 32 classes of chronic comorbid medications. A total of 8110 out of 10,127 participants with complete covariate information were included. Survival analysis adjusted for covariates showed, compared to a low medication use class, mortality was highest in participants with hypertension+diabetes+statin+antiplatelet medication group. Participants in hypertension+SSRI+statin medication group had the highest odds of AECOPD and the highest SGRQ score at both P1 and P2.Conclusion: Medication pattern can serve as a good indicator of an individual’s comorbidities profile and improves models predicting clinical outcomes.Keywords: COPDGene, co-morbidities, latent class analysis, medication patterns, mortality

وصف الملف: electronic resource

العلاقة: https://www.dovepress.com/co-morbidity-patterns-identified-using-latent-class-analysis-of-medica-peer-reviewed-article-CLEPTest; https://doaj.org/toc/1179-1349Test

الوصول الحر: https://doaj.org/article/c54e625dac5c4edfa09d0f20f9c392f5Test

المؤلفون: Lutz, SM, Frederiksen, B, Begum, F, McDonald, M-L, Cho, MH, Hobbs, B, Parker, MM, DeMeo, DL, Hersh, CP, Eringher, M, Young, K, Jiang, L, Foreman, MG, Kinney, GL, Make, BJ, Lomas, DA, Bakke, P, Gulsvik, A, Crapo, JD, Silverman, EK, Beaty, TH, Hokanson, JE

المصدر: Nicotine & Tobacco Research (2018) (In press).

مصطلحات موضوعية: smoking, chronic obstructive airway disease, chromosomes, human, pair 19, genes, genome single nucleotide polymorphism, genetics, genetic epidemiology, cigarettes, cytochrome p450 cyp2b6 enzyme, cyp2b6 gene, genome-wide association study, exome, continuing professional development, smokers

الوصف: INTRODUCTION: Cigarette smoking is a major environmental risk factor for many diseases, including chronic obstructive pulmonary disease (COPD). There are shared genetic influences on cigarette smoking and COPD. Genetic risk factors for cigarette smoking in cohorts enriched for COPD are largely unknown. METHODS: We performed genome-wide association analyses for average cigarettes per day (CPD) across the Genetic Epidemiology of COPD (COPDGene) non-Hispanic white (NHW) (n = 6659) and African American (AA) (n = 3260), GenKOLS (the Genetics of Chronic Obstructive Lung Disease) (n = 1671), and ECLIPSE (the Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints) (n = 1942) cohorts. In addition, we performed exome array association analyses across the COPDGene NHW and AA cohorts. We considered analyses across the entire cohort and stratified by COPD case–control status. RESULTS: We identified genome-wide significant associations for CPD on chromosome 15q25 across all cohorts (lowest p = 1.78 × 10⁻¹⁵), except in the COPDGene AA cohort alone. Previously reported associations on chromosome 19 had suggestive and directionally consistent associations (RAB4, p = 1.95 × 10⁻⁶; CYP2A7, p = 7.50 × 10⁻⁵; CYP2B6, p = 4.04 × 10⁻⁴). When we stratified by COPD case–control status, single nucleotide polymorphisms on chromosome 15q25 were nominally associated with both NHW COPD cases (β = 0.11, p = 5.58 × 10−4) and controls (β = 0.12, p = 3.86 × 10⁻¹⁵). For the gene-based exome array association analysis of rare variants, there were no exome-wide significant associations. For these previously replicated associations, the most significant results were among COPDGene NHW subjects for CYP2A7 (p = 5.2 × 10⁻⁴). CONCLUSIONS: In a large genome-wide association study of both common variants and a gene-based association of rare coding variants in ever-smokers, we found genome-wide significant associations on chromosome 15q25 with CPD for common variants, but not for rare coding variants. These results were directionally ...

وصف الملف: text

العلاقة: https://discovery.ucl.ac.uk/id/eprint/10060700/1/Lomas_Common%20and%20rare%20variants%20genetic%20association%20analysis%20of%20cigarettes%20per%20day%20among%20ever%20smokers%20in%20COPD%20cases%20and%20controls_AAM.pdfTest; https://discovery.ucl.ac.uk/id/eprint/10060700Test/

الإتاحة: https://discovery.ucl.ac.uk/id/eprint/10060700/1/Lomas_Common%20and%20rare%20variants%20genetic%20association%20analysis%20of%20cigarettes%20per%20day%20among%20ever%20smokers%20in%20COPD%20cases%20and%20controls_AAM.pdfTest
https://discovery.ucl.ac.uk/id/eprint/10060700Test/

المؤلفون: Lowe, KE, Regan, EA, Anzueto, A, Austin, E, Austin, JHM, Beaty, TH, Benos, PV, Benway, CJ, Bhatt, SP, Bleecker, ER, Bodduluri, S, Bon, J, Boriek, AM, Boueiz, AR, Bowler, RP, Budoff, M, Casaburi, R, Castaldi, PJ, Charbonnier, J-P, Cho, MH, Comellas, A, Conrad, D, Costa Davis, C, Criner, GJ, Curran-Everett, D, Curtis, JL, DeMeo, DL, Diaz, AA, Dransfield, MT, Dy, JG, Fawzy, A, Fleming, M, Flenaugh, EL, Foreman, MG, Fortis, S, Gebrekristos, H, Grant, S, Grenier, PA, Gu, T, Gupta, A, Han, MK, Hanania, NA, Hansel, NN, Hayden, LP, Hersh, CP, Hobbs, BD, Hoffman, EA, Hogg, JC, Hokanson, JE, Hoth, KF, Hsiao, A, Humphries, S, Jacobs, K, Jacobson, FL, Kazerooni, EA, Kim, V, Kim, WJ, Kinney, GL, Koegler, H, Lutz, SM, Lynch, DA, MacIntye, NR, Make, BJ, Marchetti, N, Martinez, FJ, Maselli, DJ, Mathews, AM, McCormack, MC, McDonald, M-LN, McEvoy, CE, Moll, M, Molye, SS, Murray, S, Nath, H, Newell, JD, Occhipinti, M, Paoletti, M, Parekh, T, Pistolesi, M, Pratte, KA, Putcha, N, Ragland, M, Reinhardt, JM, Rennard, SI, Rosiello, RA, Ross, JC, Rossiter, HB, Ruczinski, I, San Jose Estepar, R, Sciurba, FC, Sieren, JC, Singh, H, Soler, X, Steiner, RM, Strand, MJ, Stringer, WW, Tal-Singer, R, Thomashow, B, Vegas Sánchez-Ferrero, G, Walsh, JW, Wan, ES, Washko, GR, Michael Wells, J, Wendt, CH, Westney, G, Wilson, A, Wise, RA, Yen, A, Young, K, Yun, J, Silverman, EK, Crapo, JD

الوصف: Background:Chronic obstructive pulmonary disease (COPD) remains a major cause of morbidity and mortality. Present-day diagnostic criteria are largely based solely on spirometric criteria. Accumulating evidence has identified a substantial number of individuals without spirometric evidence of COPD who suffer from respiratory symptoms and/or increased morbidity and mortality. There is a clear need for an expanded definition of COPD that is linked to physiologic, structural (computed tomography [CT]) and clinical evidence of disease. Using data from the COPD Genetic Epidemiology study (COPDGene®), we hypothesized that an integrated approach that includes environmental exposure, clinical symptoms, chest CT imaging and spirometry better defines disease and captures the likelihood of progression of respiratory obstruction and mortality. Methods:Four key disease characteristics - environmental exposure (cigarette smoking), clinical symptoms (dyspnea and/or chronic bronchitis), chest CT imaging abnormalities (emphysema, gas trapping and/or airway wall thickening), and abnormal spirometry - were evaluated in a group of 8784 current and former smokers who were participants in COPDGene® Phase 1. Using these 4 disease characteristics, 8 categories of participants were identified and evaluated for odds of spirometric disease progression (FEV1 > 350 ml loss over 5 years), and the hazard ratio for all-cause mortality was examined. Results:Using smokers without symptoms, CT imaging abnormalities or airflow obstruction as the reference population, individuals were classified as Possible COPD, Probable COPD and Definite COPD. Current Global initiative for obstructive Lung Disease (GOLD) criteria would diagnose 4062 (46%) of the 8784 study participants with COPD. The proposed COPDGene® 2019 diagnostic criteria would add an additional 3144 participants. Under the new criteria, 82% of the 8784 study participants would be diagnosed with Possible, Probable or Definite COPD. These COPD groups showed increased risk of disease ...

وصف الملف: text

العلاقة: https://eprints.whiterose.ac.uk/153861/8/JCOPDF-2019-0149-Lowe.pdfTest; Lowe, KE, Regan, EA, Anzueto, A et al. (109 more authors) (2019) COPDGene® 2019: Redefining the Diagnosis of Chronic Obstructive Pulmonary Disease. Chronic Obstructive Pulmonary Diseases: Journal of the COPD Foundation, 6 (5). pp. 384-399. ISSN 2372-952X

الإتاحة: https://eprints.whiterose.ac.uk/153861Test/
https://eprints.whiterose.ac.uk/153861/8/JCOPDF-2019-0149-Lowe.pdfTest

المؤلفون: Martinez, CH, Freeman, CM, Nelson, JD, Murray, S, Wang, X, Budoff, MJ, Dransfield, MT, Hokanson, JE, Kazerooni, EA, Kinney, GL, Regan, EA, Wells, JM, Martinez, FJ, Han, MK, Curtis, JL, Investigators, C

المصدر: Respiratory research, vol 18, iss 1
Martinez, CH; Freeman, CM; Nelson, JD; Murray, S; Wang, X; Budoff, MJ; et al.(2017). GDF-15 plasma levels in chronic obstructive pulmonary disease are associated with subclinical coronary artery disease. RESPIRATORY RESEARCH, 18, 42. doi: 10.1186/s12931-017-0521-1. UCLA: Retrieved from: http://www.escholarship.org/uc/item/1f24z25pTest

مصطلحات موضوعية: Male, Adult, Chronic Obstructive, Michigan, Aging, Growth Differentiation Factor 15, Chronic Obstructive Pulmonary Disease, Clinical Sciences, Respiratory System, Comorbidity, Coronary Artery Disease, Cardiorespiratory Medicine and Haematology, Cardiovascular, Sensitivity and Specificity, Pulmonary Disease, Risk Factors, Clinical Research, Tobacco, Humans, Lung, Heart Disease - Coronary Heart Disease, Aged, COPDGene Investigators, Tobacco Smoke and Health, Cross, Incidence, Prevention, Reproducibility of Results, Middle Aged, Atherosclerosis, Sectional Studies, Causality, Cross-Sectional Studies, Heart Disease, Good Health and Well Being, Asymptomatic Diseases, Multivariate Analysis, Respiratory, Female, Biomarkers

الوصف: BackgroundGrowth differentiation factor-15 (GDF-15), a cytokine associated with cardiovascular mortality, increases during chronic obstructive pulmonary disease (COPD) exacerbations, but any role in stable COPD is unknown. We tested associations between GDF-15 and subclinical coronary atherosclerosis, assessed by coronary artery calcium (CAC) score, in COPD subjects free of clinical cardiovascular disease (CVD).MethodsCross-sectional analysis of COPD participants (GOLD stages 2-4) in the COPDGene cohort without CVD at enrollment, using baseline CAC (from non-EKG-gated chest computed tomography) and plasma GDF-15 (by custom ELISA). We used multinomial logistic modeling of GDF-15 associations with CAC, adjusting for demographics, baseline risk (calculated using the HEART: Personal Heart Early Assessment Risk Tool (Budoff et al. 114:1761-1791, 2006) score), smoking history, measures of airflow obstruction, emphysema and airway disease severity.ResultsAmong 694 participants with COPD (47% women, mean age 63.6years) mean GDF-15 was 1,304pg/mL, and mean CAC score was 198. Relative to the lower GDF-15 tertile, higher tertiles showed bivariate association with increasing CAC score (mid tertile odds ratio [OR] 1.80, 95% confidence interval [CI] 1.29, 2.51; higher tertile OR 2.86, CI 2.04, 4.02). This association was maintained after additionally adjusting for baseline CVD risk, for co-morbidities and descriptors of COPD severity and impact, markers of cardiac stress (N-terminal pro-B-type natriuretic peptide, troponin T) and of inflammation (Interleukin-6), and in subgroup analysis excluding men, diabetics, current smokers or those with limited ambulation.ConclusionsIn ever-smokers with COPD free of clinical CVD, GDF-15 contributes independently to subclinical coronary atherosclerosis.Trial registrationClinicalTrials.gov, NCT00608764 . Registered 28 January 2008.

وصف الملف: application/pdf

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=dedup_wf_001::e692e538427ef3c70794f67b7b23ce6eTest
https://escholarship.org/uc/item/1f24z25pTest

المؤلفون: Bhatt, SP, Soler, X, Wang, X, Murray, S, Anzueto, AR, Beaty, TH, Boriek, AM, Casaburi, R, Criner, GJ, Diaz, AA, Dransfield, MT, Curran-Everett, D, Galbán, CJ, Hoffman, EA, Hogg, JC, Kazerooni, EA, Kim, V, Kinney, GL, Lagstein, A, Lynch, DA, Make, BJ, Martinez, FJ, Ramsdell, JW, Reddy, R, Ross, BD, Rossiter, HB, Steiner, RM, Strand, MJ, Van Beek, EJR, Wan, ES, Washko, GR, Wells, JM, Wendt, CH, Wise, RA, Silverman, EK, Crapo, JD, Bowler, RP, Han, MK

الوصف: Background: The small conducting airways are the major site of airflow obstruction in COPD and may precede emphysema development. We hypothesized a novel CT biomarker of small airways disease predicts FEV1 decline. Methods: We analyzed 1,508 current and former smokers from COPDGene with linear regression to assess predictors of change in FEV1 (ml/year) over 5 years. Separate models for non-obstructed and obstructed subjects were generated using baseline clinical and physiologic predictors in addition to two novel CT metrics created by Parametric Response Mapping (PRM), a technique pairing inspiratory and expiratory CT images to define emphysema (PRMemph) and functional small airways disease (PRMfSAD), a measure of non-emphysematous air trapping. Results: Mean (SD) rate of FEV1 decline in ml/year for GOLD 0-4 was as follows: 41.8 (47.7), 53.8 (57.1), 45.6 (61.1), 31.6 (43.6), and 5.1 (35.8) respectively (trend test for grades 1-4, p<0.001). In multivariable linear regression, for non-obstructed participants, PRMfSAD but not PRMemph was associated with FEV1 decline, p<0.001. In GOLD 1-4 participants, both functional small airways disease (PRMfSAD) and emphysema (PRMemph) were associated with FEV1 decline (p<0.001 and p=0.001, respectively). Based on the model, the proportional contribution of the two CT metrics to FEV1 decline, relative to each other, was 87% vs. 13% and 68% vs. 32% for PRMfSAD and PRMemph in GOLD 1/2 and 3/4, respectively. Conclusions: Both CT assessed functional small airways disease and emphysema are associated with FEV1 decline, but the association with functional small airways disease has greatest importance in mild-to-moderate stage COPD where the rate of FEV1 decline is the greatest.

وصف الملف: text

العلاقة: https://eprints.whiterose.ac.uk/94612/1/PRM%20Main%20Manuscript%20for%20AJRCCM_Revised_Clean.pdfTest; Bhatt, SP, Soler, X, Wang, X et al. (35 more authors) (2016) Association between Functional Small Airway Disease and FEV1 Decline in Chronic Obstructive Pulmonary Disease. American Journal of Respiratory and Critical Care Medicine, 194 (2). pp. 178-184. ISSN 1073-449X

الإتاحة: https://doi.org/10.1164/rccm.201511-2219OCTest
https://eprints.whiterose.ac.uk/94612Test/
https://eprints.whiterose.ac.uk/94612/1/PRM%20Main%20Manuscript%20for%20AJRCCM_Revised_Clean.pdfTest

المؤلفون: Rodrigues TC, Veyna AM, Haarhues MD, Kinney GL, Rewers M, Snell-Bergeon JK, Rodrigues, Ticiana C, Veyna, Adrienne M, Haarhues, Michelle D, Kinney, Gregory L, Rewers, Marian, Snell-Bergeon, Janet K

المصدر: Diabetes Technology & Therapeutics; 2011 Oct, Vol. 13 Issue 10, p991-996, 6p

المؤلفون: Rodrigues TC, Ehrlich J, Hunter CM, Kinney GL, Rewers M, Snell-Bergeon JK, Rodrigues, Ticiana C, Ehrlich, James, Hunter, Cortney M, Kinney, Gregory L, Rewers, Marian, Snell-Bergeon, Janet K

المصدر: Diabetes Technology & Therapeutics; 2010 Dec, Vol. 12 Issue 12, p963-969, 7p