Chronic obstructive pulmonary disease phenotypes: the future of COPD.
MeiLan K. Han,Alvar Agusti,Peter M.A. Calverley,Bartolome R. Celli,Gerard J. Criner,Jeffrey L. Curtis,Leonardo M. Fabbri,Jonathan G. Goldin,Paul W. Jones,William MacNee,Barry J. Make,Klaus F. Rabe,Stephen I. Rennard,Frank C. Sciurba,Edwin K. Silverman,Jørgen Vestbo,George R. Washko,Emiel F.M. Wouters,Fernando J. Martinez +18 more
TLDR
This work proposes the following variation on this definition of COPD phenotypes: "a single or combination of disease attributes that describe differences between individuals with COPD as they relate to clinically meaningful outcomes (symptoms, exacerbations, response to therapy, rate of disease progression, or death)."Abstract:
Significant heterogeneity of clinical presentation and disease progression exists within chronic obstructive pulmonary disease (COPD). Although FEV(1) inadequately describes this heterogeneity, a clear alternative has not emerged. The goal of phenotyping is to identify patient groups with unique prognostic or therapeutic characteristics, but significant variation and confusion surrounds use of the term "phenotype" in COPD. Phenotype classically refers to any observable characteristic of an organism, and up until now, multiple disease characteristics have been termed COPD phenotypes. We, however, propose the following variation on this definition: "a single or combination of disease attributes that describe differences between individuals with COPD as they relate to clinically meaningful outcomes (symptoms, exacerbations, response to therapy, rate of disease progression, or death)." This more focused definition allows for classification of patients into distinct prognostic and therapeutic subgroups for both clinical and research purposes. Ideally, individuals sharing a unique phenotype would also ultimately be determined to have a similar underlying biologic or physiologic mechanism(s) to guide the development of therapy where possible. It follows that any proposed phenotype, whether defined by symptoms, radiography, physiology, or cellular or molecular fingerprint will require an iterative validation process in which "candidate" phenotypes are identified before their relevance to clinical outcome is determined. Although this schema represents an ideal construct, we acknowledge any phenotype may be etiologically heterogeneous and that any one individual may manifest multiple phenotypes. We have much yet to learn, but establishing a common language for future research will facilitate our understanding and management of the complexity implicit to this disease.read more
Citations
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Characterisation of COPD heterogeneity in the ECLIPSE cohort
Alvar Agusti,Peter M.A. Calverley,Bartolome R. Celli,Harvey O. Coxson,Lisa D. Edwards,David A. Lomas,William MacNee,Bruce E. Miller,S.I. Rennard,Edwin K. Silverman,Ruth Tal-Singer,Emiel F.M. Wouters,Julie C. Yates,Jørgen Vestbo +13 more
TL;DR: The clinical manifestations of COPD are highly variable and the degree of airflow limitation does not capture the heterogeneity of the disease.
Journal ArticleDOI
Acute Exacerbations of Chronic Obstructive Pulmonary Disease: Identification of Biologic Clusters and Their Biomarkers
Mona Bafadhel,S McKenna,Sarah Terry,Vijay Mistry,C Reid,Pranabashis Haldar,M McCormick,Koirobi Haldar,Tatiana Kebadze,Annelyse Duvoix,Kerstin Lindblad,Hemu Patel,Paul Rugman,Paul Dodson,Martin Jenkins,Michael A. Saunders,Paul Newbold,Ruth H. Green,Per Venge,David A. Lomas,Michael R. Barer,Sebastian L. Johnston,Ian D. Pavord,Christopher E. Brightling +23 more
TL;DR: In this paper, the authors investigated biomarker expression in COPD exacerbations to identify biologic clusters and determine biomarkers that recognize clinical exacerbation phenotypes, namely those associated with bacteria, viruses, or eosinophilic airway inflammation.
Journal ArticleDOI
Persistent systemic inflammation is associated with poor clinical outcomes in COPD: a novel phenotype.
Alvar Agusti,Lisa D. Edwards,Stephen I. Rennard,William MacNee,Ruth Tal-Singer,Bruce E. Miller,Jørgen Vestbo,Jørgen Vestbo,David A. Lomas,Peter M.A. Calverley,Emiel F.M. Wouters,Courtney Crim,Julie C. Yates,Edwin K. Silverman,Harvey O. Coxson,Per Bakke,Ruth J. Mayer,Bartolome R. Celli +17 more
TL;DR: Overall, the results identify a novel systemic inflammatory COPD phenotype that may be the target of specific research and treatment and show associations but do not prove causality.
Journal ArticleDOI
Computed tomography-based biomarker provides unique signature for diagnosis of COPD phenotypes and disease progression
Craig J. Galbán,MeiLan K. Han,Jennifer L. Boes,Komal Chughtai,Charles R. Meyer,Timothy D. Johnson,Stefanie Galbán,Alnawaz Rehemtulla,Ella A. Kazerooni,Fernando J. Martinez,Brian D. Ross +10 more
TL;DR: PRM is a versatile imaging biomarker capable of diagnosing disease extent and phenotype while providing detailed spatial information of disease distribution and location and its ability to differentiate between specific COPD phenotypes will allow for more accurate diagnosis of individual patients, complementing standard clinical techniques.
Journal ArticleDOI
Chronic Obstructive Pulmonary Disease Exacerbations in the COPDGene Study: Associated Radiologic Phenotypes
MeiLan K. Han,Ella A. Kazerooni,David A. Lynch,Lyrica X. Liu,Susan Murray,Jeffrey L. Curtis,Jeffrey L. Curtis,Gerard J. Criner,Victor Kim,Russell P. Bowler,Nicola A. Hanania,Antonio Anzueto,Barry J. Make,John E. Hokanson,James D. Crapo,Edwin K. Silverman,Fernando J. Martinez,George R. Washko +17 more
TL;DR: Greater lung emphysema and airway wall thickness were associated with COPD exacerbations, independent of the severity of airflow obstruction.
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Alfred P. Fishman,Fernando J. Martinez,Keith S. Naunheim,Steven Piantadosi,Robert A. Wise,Andrew L. Ries,Gail Weinmann,Douglas E. Wood +7 more
TL;DR: Overall, lung-volume-reduction surgery increases the chance of improved exercise capacity but does not confer a survival advantage over medical therapy, although it does yield a survival advantages for patients with both predominantly upper-lobe emphysema and low base-line exercise capacity.