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Original article
Lung function impairment, COPD hospitalisations and subsequent mortality
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  1. Judith Garcia-Aymerich1,2,3,4,
  2. Ignasi Serra Pons1,2,
  3. David M Mannino5,6,
  4. Andrea K Maas7,
  5. David P Miller8,
  6. Kourtney J Davis8
  1. 1Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain
  2. 2Municipal Institute of Medical Research (IMIM-Hospital del Mar), Barcelona, Spain
  3. 3CIBER Epidemiologia y Salud Pública (CIBERESP), Barcelona, Spain
  4. 4Department of Experimental and Health Sciences, Universitat Pompeu Fabra, Barcelona, Spain
  5. 5Department of Preventive Medicine and Environmental Health, University of Kentucky Medical Center, Lexington, Kentucky, USA
  6. 6Division of Pulmonary and Critical Care Medicine, University of Kentucky Medical Center, Lexington, Kentucky, USA
  7. 7Division of Pulmonary and Critical Care Medicine, University of South Carolina, Columbia, South Carolina, USA
  8. 8Worldwide Epidemiology, GlaxoSmithKline, Research Triangle Park, North Carolina, USA
  1. Correspondence to David M Mannino, Division of Pulmonary and Critical Care Medicine, University of Kentucky Medical Center, 800 Rose Street, MN 614, Lexington, KY 40536, USA; dmannino{at}uky.edu

Abstract

Background Hospitalisations and their sequelae comprise key morbidities in the natural history of chronic obstructive pulmonary disease (COPD). A study was undertaken to examine the associations between lung function impairment and COPD hospitalisation, and COPD hospitalisation and mortality.

Methods The analysis included a population-based sample of 20 571 participants with complete demographic, lung function, smoking, hospitalisation and mortality data, with 10-year median follow-up. Participants were classified by prebronchodilator lung function according to the modified Global Initiative on Obstructive Lung Disease (GOLD) criteria. Hospitalisations were defined by the presence of a COPD discharge diagnosis (ICD-9 codes 490–496). Incidence rate ratios (IRR) of COPD admissions and hazard ratios (HR) of mortality with respective 95% CI were calculated, adjusted for potential confounders.

Results The prevalence of modified GOLD categories was normal (36%), restricted (15%), GOLD stage 0 (22%), GOLD stage 1 (13%), GOLD stage 2 (11%) and GOLD stages 3 or 4 (3%). Adjusted IRRs (and 95% CI) indicated an increased risk of COPD hospitalisation associated with each COPD stage relative to normal lung function: 4.7 (3.7 to 6.1), 2.1 (1.6 to 2.6), 3.2 (2.6 to 4.0), 8.0 (6.4 to 10.0) and 25.5 (19.5 to 33.4) for the restricted, GOLD stage 0, GOLD stage 1, GOLD stage 2 and GOLD stages 3 or 4, respectively. Hospitalisation for COPD increased the risk of subsequent mortality (HR 2.7, 95% CI 2.5 to 3.0), controlling for severity, number of prior hospitalisations and other potential confounders. The increase in mortality associated with admission was very similar across the modified GOLD stages.

Conclusions COPD severity was associated with a higher rate of severe exacerbations requiring hospitalisation, although severe exacerbations at any stage were associated with a higher risk of short-term and long-term all-cause mortality.

  • Pulmonary disease
  • chronic obstructive
  • hospitalisation
  • mortality
  • epidemiology
  • clinical epidemiology
  • COPD epidemiology
  • COPD exacerbation

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Footnotes

  • Funding This study was funded by a research grant from GlaxoSmithKline. JG-A has a researcher contract from the Instituto de Salud Carlos III (CP05/00118), Ministry of Health, Spain. The Atherosclerosis Risk in Communities (ARIC) Study and Cardiovascular Health Study (CHS) are conducted and supported by the National Heart Lung and Blood Institute (NHLBI) in collaboration with the ARIC and CHS Investigators. This paper was not prepared in collaboration with investigators of the ARIC or the CHS and does not necessarily reflect the opinions or views of the ARIC investigators, CHS investigators or the NHLBI.

  • Competing interests DMM has served as a consultant to GlaxoSmithKline, Novartis, Pfizer, Forest, Astra-Zeneca and Boehringer-Ingelheim and has received research funding from GlaxoSmithKline, Novartis, Pfizer and Boehringer-Ingelheim. DPM was an employee of GlaxoSmithKline when this manuscript was developed. KJD is a current employee of GlaxoSmithKline. The other authors have no competing interests.

  • Provenance and peer review Not commissioned; externally peer reviewed.