Asthma Is a Risk Factor for Respiratory Exacerbations Without Increased Rate of Lung Function Decline

Five-Year Follow-up in Adult Smokers From the COPDGene Study

COPDGene Investigators

Research output: Contribution to journalArticle

Abstract

Background: Previous investigations in adult smokers from the COPDGene Study have shown that early-life respiratory disease is associated with reduced lung function, COPD, and airway thickening. Using 5-year follow-up data, we assessed disease progression in subjects who had experienced early-life respiratory disease. We hypothesized that there are alternative pathways to reaching reduced FEV1 and that subjects who had childhood pneumonia, childhood asthma, or asthma-COPD overlap (ACO) would have less lung function decline than subjects without these conditions. Methods: Subjects returning for 5-year follow-up were assessed. Childhood pneumonia was defined by self-reported pneumonia at < 16 years. Childhood asthma was defined as self-reported asthma diagnosed by a health professional at < 16 years. ACO was defined as subjects with COPD who self-reported asthma diagnosed by a health-professional at ≤ 40 years. Smokers with and those without these early-life respiratory diseases were compared on measures of disease progression. Results: Follow-up data from 4,915 subjects were examined, including 407 subjects who had childhood pneumonia, 323 subjects who had childhood asthma, and 242 subjects with ACO. History of childhood asthma or ACO was associated with an increased exacerbation frequency (childhood asthma, P <.001; ACO, P =.006) and odds of severe exacerbations (childhood asthma, OR, 1.41; ACO, OR, 1.42). History of childhood pneumonia was associated with increased exacerbations in subjects with COPD (absolute difference [β], 0.17; P =.04). None of these early-life respiratory diseases were associated with an increased rate of lung function decline or progression on CT scans. Conclusions: Subjects who had early-life asthma are at increased risk of developing COPD and of having more active disease with more frequent and severe respiratory exacerbations without an increased rate of lung function decline over a 5-year period. Trial Registry: ClinicalTrials.gov; No. NCT00608764; https://clinicaltrials.gov.

Original languageEnglish (US)
Pages (from-to)339-348
Number of pages10
JournalChest
Volume153
Issue number2
DOIs
StatePublished - Feb 1 2018

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Asthma
Lung
Chronic Obstructive Pulmonary Disease
Pneumonia
Disease Progression
Health
Registries

Keywords

  • asthma-COPD overlap
  • childhood asthma
  • childhood pneumonia
  • COPD
  • respiratory exacerbations

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine
  • Cardiology and Cardiovascular Medicine

Cite this

Asthma Is a Risk Factor for Respiratory Exacerbations Without Increased Rate of Lung Function Decline : Five-Year Follow-up in Adult Smokers From the COPDGene Study. / COPDGene Investigators.

In: Chest, Vol. 153, No. 2, 01.02.2018, p. 339-348.

Research output: Contribution to journalArticle

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title = "Asthma Is a Risk Factor for Respiratory Exacerbations Without Increased Rate of Lung Function Decline: Five-Year Follow-up in Adult Smokers From the COPDGene Study",
abstract = "Background: Previous investigations in adult smokers from the COPDGene Study have shown that early-life respiratory disease is associated with reduced lung function, COPD, and airway thickening. Using 5-year follow-up data, we assessed disease progression in subjects who had experienced early-life respiratory disease. We hypothesized that there are alternative pathways to reaching reduced FEV1 and that subjects who had childhood pneumonia, childhood asthma, or asthma-COPD overlap (ACO) would have less lung function decline than subjects without these conditions. Methods: Subjects returning for 5-year follow-up were assessed. Childhood pneumonia was defined by self-reported pneumonia at < 16 years. Childhood asthma was defined as self-reported asthma diagnosed by a health professional at < 16 years. ACO was defined as subjects with COPD who self-reported asthma diagnosed by a health-professional at ≤ 40 years. Smokers with and those without these early-life respiratory diseases were compared on measures of disease progression. Results: Follow-up data from 4,915 subjects were examined, including 407 subjects who had childhood pneumonia, 323 subjects who had childhood asthma, and 242 subjects with ACO. History of childhood asthma or ACO was associated with an increased exacerbation frequency (childhood asthma, P <.001; ACO, P =.006) and odds of severe exacerbations (childhood asthma, OR, 1.41; ACO, OR, 1.42). History of childhood pneumonia was associated with increased exacerbations in subjects with COPD (absolute difference [β], 0.17; P =.04). None of these early-life respiratory diseases were associated with an increased rate of lung function decline or progression on CT scans. Conclusions: Subjects who had early-life asthma are at increased risk of developing COPD and of having more active disease with more frequent and severe respiratory exacerbations without an increased rate of lung function decline over a 5-year period. Trial Registry: ClinicalTrials.gov; No. NCT00608764; https://clinicaltrials.gov.",
keywords = "asthma-COPD overlap, childhood asthma, childhood pneumonia, COPD, respiratory exacerbations",
author = "{COPDGene Investigators} and Hayden, {Lystra P.} and Hardin, {Megan E.} and Weiliang Qiu and Lynch, {David A.} and Strand, {Matthew J.} and {van Beek}, {Edwin J.} and Crapo, {James D.} and Silverman, {Edwin K.} and Hersh, {Craig P.} and Crapo, {James D.} and Make, {Barry J.} and Regan, {Elizabeth A.} and Silverman, {Edwin K.} and Beaty, {Terri L} and Ferdouse Begum and Boueiz, {Adel R.} and Robert Busch and Castaldi, {Peter J.} and Michael Cho and DeMeo, {Dawn L.} and Foreman, {Marilyn G.} and Eitan Halper-Stromberg and Nadia Hansel and Hardin, {Megan E.} and Hayden, {Lystra P.} and Hersh, {Craig P.} and Jacqueline Hetmanski and Hobbs, {Brian D.} and Hokanson, {John E.} and Nan Laird and Christoph Lange and Lutz, {Sharon M.} and McDonald, {Merry Lynn} and Parker, {Margaret M.} and Dandi Qiao and Regan, {Elizabeth A.} and Stephanie Santorico and Silverman, {Edwin K.} and Wan, {Emily S.} and {Al Qaisi}, Mustafa and Coxson, {Harvey O.} and Teresa Gray and Han, {Mei Lan K.} and Hoffman, {Eric A.} and Stephen Humphries and Jacobson, {Francine L.} and Judy, {Philip F.} and Kazerooni, {Ella A.} and Alex Kluiber and Lynch, {David A.}",
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T1 - Asthma Is a Risk Factor for Respiratory Exacerbations Without Increased Rate of Lung Function Decline

T2 - Five-Year Follow-up in Adult Smokers From the COPDGene Study

AU - COPDGene Investigators

AU - Hayden, Lystra P.

AU - Hardin, Megan E.

AU - Qiu, Weiliang

AU - Lynch, David A.

AU - Strand, Matthew J.

AU - van Beek, Edwin J.

AU - Crapo, James D.

AU - Silverman, Edwin K.

AU - Hersh, Craig P.

AU - Crapo, James D.

AU - Make, Barry J.

AU - Regan, Elizabeth A.

AU - Silverman, Edwin K.

AU - Beaty, Terri L

AU - Begum, Ferdouse

AU - Boueiz, Adel R.

AU - Busch, Robert

AU - Castaldi, Peter J.

AU - Cho, Michael

AU - DeMeo, Dawn L.

AU - Foreman, Marilyn G.

AU - Halper-Stromberg, Eitan

AU - Hansel, Nadia

AU - Hardin, Megan E.

AU - Hayden, Lystra P.

AU - Hersh, Craig P.

AU - Hetmanski, Jacqueline

AU - Hobbs, Brian D.

AU - Hokanson, John E.

AU - Laird, Nan

AU - Lange, Christoph

AU - Lutz, Sharon M.

AU - McDonald, Merry Lynn

AU - Parker, Margaret M.

AU - Qiao, Dandi

AU - Regan, Elizabeth A.

AU - Santorico, Stephanie

AU - Silverman, Edwin K.

AU - Wan, Emily S.

AU - Al Qaisi, Mustafa

AU - Coxson, Harvey O.

AU - Gray, Teresa

AU - Han, Mei Lan K.

AU - Hoffman, Eric A.

AU - Humphries, Stephen

AU - Jacobson, Francine L.

AU - Judy, Philip F.

AU - Kazerooni, Ella A.

AU - Kluiber, Alex

AU - Lynch, David A.

PY - 2018/2/1

Y1 - 2018/2/1

N2 - Background: Previous investigations in adult smokers from the COPDGene Study have shown that early-life respiratory disease is associated with reduced lung function, COPD, and airway thickening. Using 5-year follow-up data, we assessed disease progression in subjects who had experienced early-life respiratory disease. We hypothesized that there are alternative pathways to reaching reduced FEV1 and that subjects who had childhood pneumonia, childhood asthma, or asthma-COPD overlap (ACO) would have less lung function decline than subjects without these conditions. Methods: Subjects returning for 5-year follow-up were assessed. Childhood pneumonia was defined by self-reported pneumonia at < 16 years. Childhood asthma was defined as self-reported asthma diagnosed by a health professional at < 16 years. ACO was defined as subjects with COPD who self-reported asthma diagnosed by a health-professional at ≤ 40 years. Smokers with and those without these early-life respiratory diseases were compared on measures of disease progression. Results: Follow-up data from 4,915 subjects were examined, including 407 subjects who had childhood pneumonia, 323 subjects who had childhood asthma, and 242 subjects with ACO. History of childhood asthma or ACO was associated with an increased exacerbation frequency (childhood asthma, P <.001; ACO, P =.006) and odds of severe exacerbations (childhood asthma, OR, 1.41; ACO, OR, 1.42). History of childhood pneumonia was associated with increased exacerbations in subjects with COPD (absolute difference [β], 0.17; P =.04). None of these early-life respiratory diseases were associated with an increased rate of lung function decline or progression on CT scans. Conclusions: Subjects who had early-life asthma are at increased risk of developing COPD and of having more active disease with more frequent and severe respiratory exacerbations without an increased rate of lung function decline over a 5-year period. Trial Registry: ClinicalTrials.gov; No. NCT00608764; https://clinicaltrials.gov.

AB - Background: Previous investigations in adult smokers from the COPDGene Study have shown that early-life respiratory disease is associated with reduced lung function, COPD, and airway thickening. Using 5-year follow-up data, we assessed disease progression in subjects who had experienced early-life respiratory disease. We hypothesized that there are alternative pathways to reaching reduced FEV1 and that subjects who had childhood pneumonia, childhood asthma, or asthma-COPD overlap (ACO) would have less lung function decline than subjects without these conditions. Methods: Subjects returning for 5-year follow-up were assessed. Childhood pneumonia was defined by self-reported pneumonia at < 16 years. Childhood asthma was defined as self-reported asthma diagnosed by a health professional at < 16 years. ACO was defined as subjects with COPD who self-reported asthma diagnosed by a health-professional at ≤ 40 years. Smokers with and those without these early-life respiratory diseases were compared on measures of disease progression. Results: Follow-up data from 4,915 subjects were examined, including 407 subjects who had childhood pneumonia, 323 subjects who had childhood asthma, and 242 subjects with ACO. History of childhood asthma or ACO was associated with an increased exacerbation frequency (childhood asthma, P <.001; ACO, P =.006) and odds of severe exacerbations (childhood asthma, OR, 1.41; ACO, OR, 1.42). History of childhood pneumonia was associated with increased exacerbations in subjects with COPD (absolute difference [β], 0.17; P =.04). None of these early-life respiratory diseases were associated with an increased rate of lung function decline or progression on CT scans. Conclusions: Subjects who had early-life asthma are at increased risk of developing COPD and of having more active disease with more frequent and severe respiratory exacerbations without an increased rate of lung function decline over a 5-year period. Trial Registry: ClinicalTrials.gov; No. NCT00608764; https://clinicaltrials.gov.

KW - asthma-COPD overlap

KW - childhood asthma

KW - childhood pneumonia

KW - COPD

KW - respiratory exacerbations

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U2 - 10.1016/j.chest.2017.11.038

DO - 10.1016/j.chest.2017.11.038

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VL - 153

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JO - Chest

JF - Chest

SN - 0012-3692

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