Abstract

The aim of this systematic review and meta-analysis was to assess the blood concentrations of the total and reduced forms of the low-molecular-weight antioxidant thiol glutathione (GSH) in chronic obstructive pulmonary disease (COPD) patients in comparison to healthy individuals. A literature search was conducted in the PubMed and Web of Science databases from inception until June 2020. In the 18 studies identified (involving a total of 974 COPD patients and 631 healthy controls), the pooled reduced GSH concentrations were significantly lower in patients with COPD than controls (SMD = −3.04, 95% CI = −4.42 to −1.67; p < 0.001). By contrast, the pooled total GSH concentrations were significantly higher in patients with COPD than controls (SMD = 0.42, 95% CI = 0.11 to 0.73; p = 0.009). Our meta-analysis showed that the blood concentrations of reduced GSH, even in the presence of higher total GSH concentrations, were significantly lower in patients with COPD when compared to healthy controls. This suggests that an impaired antioxidant defense system plays an important role in the pathogenesis of COPD.

Highlights

  • Chronic obstructive pulmonary disease (COPD), a non-communicable respiratory disease with an estimated prevalence of 4–20% in adults over 40 years worldwide, is characterized by progressive airflow limitation and emphysematous changes in the lungs [1,2]

  • Pooled analysis showed that chronic obstructive pulmonary disease (COPD) patients have significantly lower reduced GSH (rGSH), and higher total GSH (tGSH), concentrations when compared to healthy controls

  • The association observed between the pooled GSH standardized mean differences (SMDs) and MDA concentrations in the meta-regression analysis (t = −3.40, p = 0.009, Figure 6) supports this proposition, as an increase in plasma MDA concentrations is common in patients with advanced COPD [56,57]

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Summary

Introduction

Chronic obstructive pulmonary disease (COPD), a non-communicable respiratory disease with an estimated prevalence of 4–20% in adults over 40 years worldwide, is characterized by progressive airflow limitation and emphysematous changes in the lungs [1,2]. Oxidative stress, resulting from an excess of oxidants and/or a deficit in antioxidant defense mechanisms, favors lung tissue damage and activates specific molecular mechanisms that initiate local inflammation [8]. The latter involves the activation of epithelial cells and resident macrophages, and the recruitment and activation of neutrophils, eosinophils, monocytes and lymphocytes that release a variety of pro-inflammatory mediators, including cytokines, chemokines, growth factors and lipid mediators [4].

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