Egyptian Journal of Chest Disease and Tuberculosis (Jul 2016)

The impact of smoking on inflammatory biomarkers in patients with chronic obstructive pulmonary disease

  • Yasser A. Korani,
  • Alaa T. Hassan,
  • Effat A.E. Tony,
  • Madleen Adel A. Abdou

DOI
https://doi.org/10.1016/j.ejcdt.2016.04.011
Journal volume & issue
Vol. 65, no. 3
pp. 597 – 603

Abstract

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Background: Chronic obstructive pulmonary disease (COPD) is a chronic progressive inflammatory disease characterized by airflow limitation that is not fully reversible (Nillawar et al., 2012). The pathophysiology of COPD is not completely understood. Cigarette smoking is a major risk factor for chronic obstructive pulmonary disease (COPD). Elevated CRP has been increasingly used as a surrogate marker of systemic inflammation in diverse conditions. TNF-α, a powerful pro-inflammatory cytokine primarily produced by activated macrophages, is thought to play a critical role in the pathogenesis of COPD (Higashimoto et al., 2008; Churg et al., 2002). The aim of the work: To evaluate the impact of smoking on inflammatory biomarkers and relations between these biomarkers and the decline of lung function in COPD patients. Methods: This case–control observational prospective study was conducted on fifty-eight clinically stable COPD patients (26 non-smokers and 32 current smokers; at different stages ranged from mild to very severe), their mean age 53.1 ± 14.25 and 53.9 ± 5.95 years respectively), recruited from Chest Department, Assiut University Hospitals. All patients met the Global Initiative for Obstructive Lung Disease (GOLD) (Battaglia et al., 2007). All participants were subjected to thorough history taking, full clinical examination, anthropometric measurements with spirometry and chest X-ray. Peripheral hemogram, liver function tests, kidney function tests, high sensitivity C-reactive protein (hs CRP) and serum level of TNF-α were measured for both patients and controls. Results: The concentrations of circulating hs-CRP and TNF-α, were highly significantly elevated in patients with COPD in comparison to the control group (3.74 ± 0.2 vs. 1.30 ± 0.14 for hs-CRP; 33.88 ± 5.97 vs. 8.79 ± 0. 57 for TNF-α with p 0.05). Interestingly, there were significant negative correlations between the levels of TNF-α and hs-CRP, and FEV1 in stages II, III, and IV of COPD. Conclusions: The circulating levels of the inflammatory markers hs-CRP and TNF-alpha are significantly elevated in patients with stable COPD and these biomarkers could be used as predictor factors for severity of inflammation in COPD patients. Longitudinal studies evaluating the effects of smoking cessation on bronchial and systemic inflammation are needed to allow better understanding of these relationships and their consequences.

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