Childhood pneumonia increases risk for chronic obstructive pulmonary disease: the COPDGene study

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Abstract

Background

Development of adult respiratory disease is influenced by events in childhood. The impact of childhood pneumonia on chronic obstructive pulmonary disease (COPD) is not well defined. We hypothesize that childhood pneumonia is a risk factor for reduced lung function and COPD in adult smokers.

Methods

COPD cases and control smokers between 45–80 years old from the United States COPDGene Study were included. Childhood pneumonia was defined by self-report of pneumonia at <16 years. Subjects with lung disease other than COPD or asthma were excluded. Smokers with and without childhood pneumonia were compared on measures of respiratory disease, lung function, and quantitative analysis of chest CT scans.

Results

Of 10,192 adult smokers, 854 (8.4 %) reported pneumonia in childhood. Childhood pneumonia was associated with COPD (OR 1.40; 95 % CI 1.17-1.66), chronic bronchitis, increased COPD exacerbations, and lower lung function: post-bronchodilator FEV ₁ (69.1 vs. 77.1 % predicted), FVC (82.7 vs. 87.4 % predicted), FEV ₁/FVC ratio (0.63 vs. 0.67; p < 0.001 for all comparisons). Childhood pneumonia was associated with increased airway wall thickness on CT, without significant difference in emphysema. Having both pneumonia and asthma in childhood further increased the risk of developing COPD (OR 1.85; 95 % CI 1.10-3.18).

Conclusions

Children with pneumonia are at increased risk for future smoking-related lung disease including COPD and decreased lung function. This association is supported by airway changes on chest CT scans. Childhood pneumonia may be an important factor in the early origins of COPD, and the combination of pneumonia and asthma in childhood may pose the greatest risk.

Clinical trials registration

ClinicalTrials.gov, NCT00608764 (Active since January 28, 2008).

Electronic supplementary material

The online version of this article (doi:10.1186/s12931-015-0273-8) contains supplementary material, which is available to authorized users.

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Most cited references 23

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Epidemiology Standardization Project (American Thoracic Society).

B G Ferris (1978)

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Epidemiology, genetics, and subtyping of preserved ratio impaired spirometry (PRISm) in COPDGene

Emily S Wan, Peter J Castaldi, Michael Cho … (2014)

Background Preserved Ratio Impaired Spirometry (PRISm), defined as a reduced FEV1 in the setting of a preserved FEV1/FVC ratio, is highly prevalent and is associated with increased respiratory symptoms, systemic inflammation, and mortality. Studies investigating quantitative chest tomographic features, genetic associations, and subtypes in PRISm subjects have not been reported. Methods Data from current and former smokers enrolled in COPDGene (n = 10,192), an observational, cross-sectional study which recruited subjects aged 45–80 with ≥10 pack years of smoking, were analyzed. To identify epidemiological and radiographic predictors of PRISm, we performed univariate and multivariate analyses comparing PRISm subjects both to control subjects with normal spirometry and to subjects with COPD. To investigate common genetic predictors of PRISm, we performed a genome-wide association study (GWAS). To explore potential subgroups within PRISm, we performed unsupervised k-means clustering. Results The prevalence of PRISm in COPDGene is 12.3%. Increased dyspnea, reduced 6-minute walk distance, increased percent emphysema and decreased total lung capacity, as well as increased segmental bronchial wall area percentage were significant predictors (p-value <0.05) of PRISm status when compared to control subjects in multivariate models. Although no common genetic variants were identified on GWAS testing, a significant association with Klinefelter’s syndrome (47XXY) was observed (p-value < 0.001). Subgroups identified through k-means clustering include a putative “COPD-subtype”, “Restrictive-subtype”, and a highly symptomatic “Metabolic-subtype”. Conclusions PRISm subjects are clinically and genetically heterogeneous. Future investigations into the pathophysiological mechanisms behind and potential treatment options for subgroups within PRISm are warranted. Trial registration Clinicaltrials.gov Identifier: NCT000608764. Electronic supplementary material The online version of this article (doi:10.1186/s12931-014-0089-y) contains supplementary material, which is available to authorized users.

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Asthma as a risk factor for COPD in a longitudinal study.

Stefano Guerra, R R Barbee, J L Sherrill … (2004)

For several years, asthma and COPD have been regarded as distinct entities, with distinct clinical courses. However, despite distinctive physiologic features at the time of diagnosis, and different risk factors, the two diseases over time may develop features that are quite similar. To evaluate the association between physician-diagnosed asthma and the subsequent development of COPD in a cohort of 3,099 adult subjects from Tucson, AZ. A prospective observational study. Participants completed up to 12 standard respiratory questionnaires and 11 spirometry lung function measurements over a period of 20 years. Survival curves (with time to development of COPD as the dependent variable) were compared between subjects with asthma and subjects without asthma at the initial survey. Subjects with active asthma (n = 192) had significantly higher hazard ratios than inactive (n = 156) or nonasthmatic subjects (n = 2751) for acquiring COPD. As compared with nonasthmatics, active asthmatics had a 10-times-higher risk for acquiring symptoms of chronic bronchitis (95% confidence interval [CI], 4.94 to 20.25), 17-times-higher risk of receiving a diagnosis of emphysema (95% CI, 8.31 to 34.83), and 12.5-times-higher risk of fulfilling COPD criteria (95% CI, 6.84 to 22.84), even after adjusting for smoking history and other potential confounders. Physician-diagnosed asthma is significantly associated with an increased risk for CB, emphysema, and COPD.

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Author and article information

Contributors

Lystra P. Hayden: 617-525-0874 , Lystra.Hayden@childrens.harvard.edu

Brian D. Hobbs: brian.hobbs@channing.harvard.edu

Robyn T. Cohen: Robyn.Cohen@bmc.org

Robert A. Wise: rwise@jhmi.edu

William Checkley: wcheckl1@jhmi.edu

James D. Crapo: CrapoJ@njhealth.org

Craig P. Hersh: craig.hersh@channing.harvard.edu

Journal

Journal ID (nlm-ta): Respir Res

Journal ID (iso-abbrev): Respir. Res

Title: Respiratory Research

Publisher: BioMed Central (London )

ISSN (Print): 1465-9921

ISSN (Electronic): 1465-993X

Publication date (Electronic): 21 September 2015

Publication date PMC-release: 21 September 2015

Publication date (Print): 2015

Volume: 16

Issue: 1

Electronic Location Identifier: 115

Affiliations

[ ]Division of Respiratory Diseases, Boston Children’s Hospital, 300 Longwood Ave., Boston, MA 02115 USA

[ ]Channing Division of Network Medicine, Brigham and Women’s Hospital, 181 Longwood Ave., Boston, MA 02115 USA

[ ]Division of Pulmonary and Critical Care Medicine, Brigham and Women’s Hospital, 75 Francis St., Boston, MA 02115 USA

[ ]Department of Pediatrics, Boston University School of Medicine, 72 E Concord St., Boston, MA 02118 USA

[ ]Division of Pulmonary and Critical Care, Johns Hopkins University School of Medicine, 1830 E. Monument St., Baltimore, MD 21205 USA

[ ]Department of Medicine, National Jewish Health, 1400 Jackson St., Denver, CO 80206 USA

Article

Publisher ID: 273

DOI: 10.1186/s12931-015-0273-8

PMC ID: 4578796

PubMed ID: 26392057

SO-VID: c5622fe0-1cd3-4748-ab76-6bd7130d821d

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 14 July 2015

Date accepted : 6 September 2015

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Childhood pneumonia increases risk for chronic obstructive pulmonary disease: the COPDGene study

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Abstract

Background

Methods

Results

Conclusions

Clinical trials registration

Electronic supplementary material

Related collections

Inflamed lung in vitro co-culture models

Most cited references 23

Epidemiology Standardization Project (American Thoracic Society).

Epidemiology, genetics, and subtyping of preserved ratio impaired spirometry (PRISm) in COPDGene

Asthma as a risk factor for COPD in a longitudinal study.

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Cited by 26

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