Exhaled Ethane, a Marker of Lipid Peroxidation, Is  Elevated in Chronic Obstructive Pulmonary Disease

Paredi, Paolo; Kharitonov, Sergei A.; Leak, David J.; Ward, Simon; Cramer, D. A.; Barnes, Peter J.

doi:10.1164/ajrccm.162.2.9909025

Cited by 264 publications

(171 citation statements)

References 30 publications

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“…We have observed no change in eCO during hospitalization indicating that the treatment of or recovery from an exacerbation is not mirrored in eCO levels in patients with COPD. This is reminiscent to some earlier findings where no difference in eCO was found in stable COPD patients with and without corticosteroid treatments (20). Similarly, in subjects with asthma, there was no difference in eCO between patients who were taking ICS and those who were not (22).…”

Section: Discussionsupporting

confidence: 82%

“…Identification was performed on all potentially pathogenic microorganisms (PPMs) including Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Pseudomonas aeruginosa according to standardized protocols (10). Since the significance of other bacteria such as Staphylococcus aureus and Haemophilus parainfluenzae is debated (20), these agents were not considered as PPMs. Similarly, other bacterial species in sputum were classified as normal flora, in line with other studies (27).…”

Section: Sputum Bacterial Culturementioning

confidence: 99%

“…Several recent studies have reported the elevated levels of eCO in COPD as well (18,20). However, eCO levels may also be elevated in healthy smokers due to the high CO content of cigarette smoke (6,7).…”

Section: Introductionmentioning

confidence: 99%

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Assessment of exhaled carbon monoxide in exacerbations of chronic obstructive pulmonary disease

2016

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Introduction: Exhaled carbon monoxide (eCO) has been widely implicated as a pulmonary biomarker in respiratory diseases. The aim of this study was to investigate whether the treatment of patients with severe acute exacerbation of chronic obstructive pulmonary disease (AECOPD) could be aided by monitoring the changes in eCO. Methods: The levels of eCO along with routine clinical parameters were analyzed in 29 current smoker and 33 ex-smoker COPD patients, first at the time of hospital admission, and again at discharge following the standard treatment. Patients with AECOPD were also stratified according to sputum bacteria. Results: At exacerbation, the levels of eCO were increased in current smokers compared to ex-smokers (6.0 [2.0-9.5] versus 1.0 [1.0-2.0] ppm, p < 0.001). Similarly, eCO levels were higher in smokers after treatment (7.0 [2.0-12.5] versus 1.0 [1.0-2.0] ppm, p < 0.001). Treatment of AECOPD did not affect eCO concentrations. The levels of eCO were not statistically different between bacterial and non-bacterial AECOPD either. Investigating a subgroup of current smoker patients (n = 15), there was a significant correlation between the levels of eCO and blood carboxyhemoglobin concentrations both at exacerbation and discharge. No associations were found between eCO and lung function or blood gas parameters. Conclusion: Our results suggest that monitoring eCO during the treatment of AECOPD is of limited clinical value.

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Section: Discussionsupporting

confidence: 82%

Section: Sputum Bacterial Culturementioning

confidence: 99%

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Assessment of exhaled carbon monoxide in exacerbations of chronic obstructive pulmonary disease

2016

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“…Lipid peroxidation of polyunsaturated membrane fatty acids results from activated ROS released by immune and inflammatory cells. The detrimental consequences of membrane lipid peroxidation involve impairment of membrane function, inactivation of membranebound receptors and enzymes, and increased tissue permeability (Paredi et al, 2000). The most widely used marker of lipid peroxidation is malondialdehyde (MDA).…”

Section: Lipid Peroxidationmentioning

confidence: 99%

“…Chronic elevations of ethane in smokers are likely related to oxidative damage in the lungs as indicated by a highly significant correlation between ethane levels and the degree of airway obstruction in COPD (Paredi et al, 2000).…”

Section: Lipid Peroxidationmentioning

confidence: 99%

The role of oxidative stress in lung injury induced by cigarette smoke

Kluchová

Tkáčová

2006

Biologia

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Oxidative stress is a damaging process resulting from an imbalance between excessive generation of oxidant compounds and insufficient antioxidant defence mechanisms. Oxidative stress plays a crucial role in the initiation and progression of cigarette smoke-induced lung injury, deterioration in lung functions, and development of chronic obstructive pulmonary disease (COPD). In smokers and in patients with COPD, the increased oxidant burden derives from cigarette smoke per se, and from activated inflammatory cells releasing enhanced amounts of reactive oxygen and nitrogen species (ROS, RNS, respectively). Although mild oxidative stress resulting from cigarette smoking leads to the upregulation of the antioxidative enzymes synthesis in the lungs, high levels of ROS and RNS observed in patients with COPD overwhelm the antioxidant enzymes capacities, resulting in oxidant-mediated lung injury and cell death. In addition, depletion of antioxidative systems in the systemic circulation was consistently observed in such patients. The imbalance between the generation of ROS/RNS and antioxidant capacities -the state of "oxidative stress" -is one of the major pathophysiologic hallmarks in the development of COPD. Detrimental effects of oxidative stress include impairment of membrane functions, inactivation of membrane-bound receptors and enzymes, and increased tissue permeability. In addition, oxidative stress aggravates the inflammatory processes in the lungs, and contributes to the worsening of the protease-antiprotease imbalance. Several markers of oxidative stress, such as increases in lipid peroxidation products and reductions in glutathione peroxidase activity, have been shown to be related to the reductions in pulmonary functions. In the present article we review the current knowledge about the vicious cycle of cigarette smoking, oxidative stress, and inflammation in the pathogenesis of COPD.

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