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. 2011 Aug 31;6(4):214-9.
doi: 10.1186/2049-6958-6-4-214.

Systemic inflammation in COPD in relation to smoking status

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Systemic inflammation in COPD in relation to smoking status

Danielius Serapinas et al. Multidiscip Respir Med. .

Abstract

Background and aims: Smoking is the main risk factor for the development of chronic obstructive pulmonary disease (COPD) that has been recently defined as a systemic pulmonary inflammatory disease. However, the impact of smoking itself on systemic inflammation in COPD patients has not yet been well established. The aim of our study was to investigate the association between inflammatory markers and smoking status.

Materials and methods: We compared 202 current smokers, 61 ex-smokers and 57 never-smokers, all COPD patients. Assessments included medical history, spirometry, alpha-1 antitrypsin (AAT) genotyping, serum AAT, C-reactive protein (CRP), tumor necrosis factor (TNF)-α, and soluble tumor necrosis factor receptor (sTNFR)-1 and sTNFR-2 concentrations.

Results: AAT and CRP concentrations in smokers (1.75 ± 0.51 g/L and 14.4 [9.5-20.5] mg/L) and ex-smokers (1.69 ± 0.43 g/L and 12.3 [8.7-16.3] mg/L) were higher than in never-smokers (1.49 ± 0.38 g/L and 5.1 [2.5-8.7] mg/L; p < 0.05). sTNFR-1 level was higher in smokers than ex-smokers or never-smokers (241.2 pg/mL [145.3-349.4] vs. 213.7 pg/mL [147.1-280.3] and 205.2 pg/mL [125-275]; p < 0.05).

Conclusions: Our data confirm that smoking is associated with increased levels of AAT, CRP, and sTNFR-1 in COPD patients, an array of systemic inflammation markers that continue to be active even after smoking cessation.

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Figures

Figure 1
Figure 1
Serum AAT concentration in COPD smokers, ex-smokers and never-smokers. Definition of abbreviation: AAT, alpha-1 antitrypsin. Data are presented as mean ± SD.
Figure 2
Figure 2
Serum CRP concentration in COPD smokers, ex-smokers and never-smokers. Definition of abbreviation: CRP, C-reactive protein. Data are presented as median (25th-75th percentile).
Figure 3
Figure 3
Serum sTNFR-1 concentration in COPD smokers, ex-smokers and never-smokers. Definition of abbreviation: sTNFR-1, soluble tumor necrosis factor α receptor 1. Data are presented as median (25th-75th percentile).

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References

    1. Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2006. Global strategy for the diagnosis, management, and prevention of COPD. Executive Summary. http://www.goldcopd.org - PubMed
    1. Willemse BW, Postma DS, Timens W, ten Hacken NH. The impact of smoking cessation on respiratory symptoms, lung function, airway hyperresponsiveness and inflammation. Eur Respir J. 2004;23:464–476. doi: 10.1183/09031936.04.00012704. - DOI - PubMed
    1. Chung KF. Cytokines as targets in chronic obstructive pulmonary disease. Curr Drug Targets. 2006;7:675–681. doi: 10.2174/138945006777435263. - DOI - PubMed
    1. Gan WQ, Man SF, Senthilselvan A, Sin DD. Association between chronic obstructive pulmonary disease and systemic inflammation: a systematic review and a meta-analysis. Thorax. 2004;59:574–580. doi: 10.1136/thx.2003.019588. - DOI - PMC - PubMed
    1. Garcia-Rio F, Miravitlles M, Soriano JB, Muñoz L, Duran-Tauleria E, Sánchez G, Sobradillo V, Ancochea J. EPI-SCAN Steering Committee. Systemic inflammation in chronic obstructive pulmonary disease: a population-based study. Respir Res. 2010;11:63. - PMC - PubMed