Risk of community-acquired pneumonia in chronic obstructive pulmonary disease stratified by smoking status: a population-based cohort study in the United Kingdom
Authors Braeken DCW, Rohde GGU, Franssen FME, Driessen JHM, van Staa TP, Souverein PC, Wouters EFM, de Vries F
Received 31 March 2017
Accepted for publication 18 May 2017
Published 14 August 2017 Volume 2017:12 Pages 2425—2432
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Charles Downs
Peer reviewer comments 3
Editor who approved publication: Dr Richard Russell
Dionne CW Braeken,1–3 Gernot GU Rohde,2 Frits ME Franssen,1,2 Johanna HM Driessen,3–5 Tjeerd P van Staa,3,6 Patrick C Souverein,3 Emiel FM Wouters,1,2 Frank de Vries3,4,7
1Department of Research and Education, CIRO, Horn, 2Department of Respiratory Medicine, Maastricht University Medical Centre (MUMC+), Maastricht, 3Division of Pharmacoepidemiology and Clinical Pharmacology, Utrecht Institute of Pharmaceutical Sciences, Utrecht, 4Department of Clinical Pharmacy and Toxicology, Maastricht University Medical Centre (MUMC+), Maastricht, 5Department of Epidemiology, Care and Public Health Research Institute (CAPHRI), Maastricht, the Netherlands; 6Department of Health eResearch, University of Manchester, Manchester, 7MRC Lifecourse Epidemiology Unit, Southampton General Hospital, Southampton, UK
Background: Smoking increases the risk of community-acquired pneumonia (CAP) and is associated with the development of COPD. Until now, it is unclear whether CAP in COPD is due to smoking-related effects, or due to COPD pathophysiology itself.
Objective: To evaluate the association between COPD and CAP by smoking status.
Methods: In total, 62,621 COPD and 191,654 control subjects, matched by year of birth, gender and primary care practice, were extracted from the Clinical Practice Research Datalink (2005–2014). Incidence rates (IRs) were estimated by dividing the total number of CAP cases by the cumulative person-time at risk. Time-varying Cox proportional hazard models were used to estimate the hazard ratios (HRs) for CAP in COPD patients versus controls. HRs of CAP by smoking status were calculated by stratified analyses in COPD patients versus controls and within both subgroups with never smoking as reference.
Results: IRs of CAP in COPD patients (32.00/1,000 person-years) and controls (6.75/1,000 person-years) increased with age and female gender. The risk of CAP in COPD patients was higher than in controls (HR 4.51, 95% CI: 4.27–4.77). Current smoking COPD patients had comparable CAP risk (HR 0.92, 95% CI: 0.82–1.02) as never smoking COPD patients (reference), whereas current smoking controls had a higher risk (HR 1.23, 95% CI: 1.13–1.34) compared to never smoking controls.
Conclusion: COPD patients have a fourfold increased risk to develop CAP, independent of smoking status. Identification of factors related with the increased risk of CAP in COPD is warranted, in order to improve the management of patients at risk.
Keywords: COPD, respiratory infections, incidence, smoking risk
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