STUDY OBJECTIVE: To investigate which cells are the main source of hydrogen peroxide (H(2)O(2)) production in stable patients with asthma and the associations among H(2)O(2) levels, airway inflammation, and disease severity. SETTING: Inpatient respiratory unit and outpatient clinic in tertiary-care hospital. PATIENTS: Fifty stable asthmatic patients with disease severity ranging from mild to moderate. METHODS: H(2)O(2) was measured in expired breath condensate and was correlated with variables expressing both asthma severity (ie, FEV(1) percent predicted, peak expiratory flow rate [PEFR] variability, symptom score, and histamine airways responsiveness) and airway inflammation (ie, differential cell counts from induced sputum and levels of eosinophil cationic protein [ECP]). RESULTS: The mean (95% confidence interval [CI]) concentration of H(2)O(2) was significantly elevated in patients with asthma compared to that in control subjects (mean, 0.67 microM [95% CI, 0.56 to 0.77 microM] vs 0.2 microM [95% CI, 0.16 to 0.24 microM]; p < 0.0001). The difference was primarily due to the elevation of H(2)O(2) in patients with moderate asthma whose expired breath H(2)O(2) level of 0.95 microM (95% CI, 0.76 to 1.12 microM) was significantly higher from that of patients with mild-persistent and mild-intermittent asthma (mean, 0.59 microM [95% CI, 0.47 to 0.7 microM] and 0.27 [95% CI, 0.23 to 0.32 microM], respectively; p < 0.0001). H(2)O(2) concentration was positively related to sputum eosinophilia as well as to ECP concentration. A similar correlation was found between H(2)O(2) and neutrophils in patients with moderate asthma. A positive correlation was observed between H(2)O(2) level, symptom score, and PEFR variability. H(2)O(2) level was negatively related to FEV(1) percent predicted. Further analysis showed that only patients with moderate asthma who were not receiving inhaled steroids were found to have a strong relationship with the variables tested. CONCLUSIONS: Eosinophils are the predominate cells that generate H(2)O(2) in all forms of the disease, while neutrophils might be responsible for the highest levels that are observed in the more severe forms of the disease. The role of H(2)O(2) concentration in predicting the severity of the disease as well as in the inflammatory process is limited and depends on the use of inhaled steroid therapy and the classification of the severity of the disease.
STUDY OBJECTIVE: To investigate which cells are the main source of hydrogen peroxide (H(2)O(2)) production in stable patients with asthma and the associations among H(2)O(2) levels, airway inflammation, and disease severity. SETTING: Inpatient respiratory unit and outpatient clinic in tertiary-care hospital. PATIENTS: Fifty stable asthmatic patients with disease severity ranging from mild to moderate. METHODS:H(2)O(2) was measured in expired breath condensate and was correlated with variables expressing both asthma severity (ie, FEV(1) percent predicted, peak expiratory flow rate [PEFR] variability, symptom score, and histamine airways responsiveness) and airway inflammation (ie, differential cell counts from induced sputum and levels of eosinophil cationic protein [ECP]). RESULTS: The mean (95% confidence interval [CI]) concentration of H(2)O(2) was significantly elevated in patients with asthma compared to that in control subjects (mean, 0.67 microM [95% CI, 0.56 to 0.77 microM] vs 0.2 microM [95% CI, 0.16 to 0.24 microM]; p < 0.0001). The difference was primarily due to the elevation of H(2)O(2) in patients with moderate asthma whose expired breath H(2)O(2) level of 0.95 microM (95% CI, 0.76 to 1.12 microM) was significantly higher from that of patients with mild-persistent and mild-intermittent asthma (mean, 0.59 microM [95% CI, 0.47 to 0.7 microM] and 0.27 [95% CI, 0.23 to 0.32 microM], respectively; p < 0.0001). H(2)O(2) concentration was positively related to sputum eosinophilia as well as to ECP concentration. A similar correlation was found between H(2)O(2) and neutrophils in patients with moderate asthma. A positive correlation was observed between H(2)O(2) level, symptom score, and PEFR variability. H(2)O(2) level was negatively related to FEV(1) percent predicted. Further analysis showed that only patients with moderate asthma who were not receiving inhaled steroids were found to have a strong relationship with the variables tested. CONCLUSIONS: Eosinophils are the predominate cells that generate H(2)O(2) in all forms of the disease, while neutrophils might be responsible for the highest levels that are observed in the more severe forms of the disease. The role of H(2)O(2) concentration in predicting the severity of the disease as well as in the inflammatory process is limited and depends on the use of inhaled steroid therapy and the classification of the severity of the disease.
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