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Persistent Systemic Inflammation is Associated with Poor Clinical Outcomes in COPD: A Novel Phenotype

Research output: Contribution to journalArticle

  • Alvar Agustí
  • Lisa D Edwards
  • Stephen I Rennard
  • William Macnee
  • Ruth Tal-Singer
  • Bruce E Miller
  • Jørgen Vestbo
  • David A Lomas
  • Peter M A Calverley
  • Emiel Wouters
  • Courtney Crim
  • Julie C Yates
  • Edwin K Silverman
  • Harvey O Coxson
  • Per Bakke
  • Ruth J Mayer
  • Bartolome Celli
  • for the Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints (ECLIPSE) Investigators

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    Rights statement: Copyright: © 2012 Agustí et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0037483
Original languageEnglish
Pages (from-to)e37483
JournalPLoS ONE
Volume7
Issue number5
DOIs
Publication statusPublished - 2012

Abstract

BACKGROUND: Because chronic obstructive pulmonary disease (COPD) is a heterogeneous condition, the identification of specific clinical phenotypes is key to developing more effective therapies. To explore if the persistence of systemic inflammation is associated with poor clinical outcomes in COPD we assessed patients recruited to the well-characterized ECLIPSE cohort (NCT00292552). METHODS AND FINDINGS: Six inflammatory biomarkers in peripheral blood (white blood cells (WBC) count and CRP, IL-6, IL-8, fibrinogen and TNF-α levels) were quantified in 1,755 COPD patients, 297 smokers with normal spirometry and 202 non-smoker controls that were followed-up for three years. We found that, at baseline, 30% of COPD patients did not show evidence of systemic inflammation whereas 16% had persistent systemic inflammation. Even though pulmonary abnormalities were similar in these two groups, persistently inflamed patients during follow-up had significantly increased all-cause mortality (13% vs. 2%, p

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