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S K Agarwal Department of Chest Diseases, Banaras Hindu University, Varanasi 221 005, India
Send letter to journal:
sk_agarwal{at}satyam.net.in S K Agarwal
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The authors have concluded that the increase of exhaled nitric oxide (NO) in patients with chronic bronchitis was similar to that seen in patients with asthma [1] and that both the diseases have common features of inflammation. Though, we know [2] that both chronic bronchitis and bronchial asthma are characterized by chronic persistent inflammatory process and the nature of the inflammation differs markedly. Airway inflammation in asthma is characterized by an eosinophilic inflammation affecting all the airways but not lung parenchyma. In chronic bronchitis, there is predominantly neutrophilic inflammation in the airways. The increased exhaled NO in asthma is related to eosinophilic inflammation of the airways and is increased during the late response to allergen and during exacerbations and is decreased by treatment with inhaled corticosteroids[3]. As authors got increased exhaled nitric oxide in chronic bronchitis, they should have gone for sputum induction and measured eosinophils and eosinophil cationic protein (ECP) in induced sputum of the patients. Sputum induction has been advocated as a non-invasive alternative method for measuring airway inflammation with greater advantage in terms of reproducibility and simplicity. Airway inflammation in asthma is characterized by increase in activated and degranulating eosinophils in induced sputum whereas chronic bronchitis is characterized by increase in granulocyte markers of neutrophil inflammation, namely myeloperoxidase and human neutrophil lectin. Moreover, there are other indices of inflammation also like – a) hydrogen peroxide in exhaled breath condensate b) serum levels of ECP and c) urinary leukotriene E4 levels. References : 1. Delen FM, Sippei JM, Osborne ML, Law S, Thukkani N, Holden WE. Increased Exhaled Nitric Oxide in Chronic Bronchitis. Chest 2000;117:695- 701 2. Barnes PJ. Mechanisms in COPD: Differences from asthma. Chest 2000;117:10S-14S. 3. Barnes PJ, Chung KF, Page CP. Inflammatory Mediators of Asthma : An Update. Pharmacological Reviews 1998;50:515-596. |
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S K Agarwal Department of Chest Diseases, Banaras Hindu University, Varanasi 221 005, India
Send letter to journal:
sk_agarwal{at}satyam.net.in S K Agarwal
|
The authors have concluded that the increase of exhaled nitric oxide (NO) in patients with chronic bronchitis was similar to that seen in patients with asthma [1] and that both the diseases have common features of inflammation. Though, we know [2] that both chronic bronchitis and bronchial asthma are characterized by chronic persistent inflammatory process and the nature of the inflammation differs markedly. Airway inflammation in asthma is characterized by an eosinophilic inflammation affecting all the airways but not lung parenchyma. In chronic bronchitis, there is predominantly neutrophilic inflammation in the airways. The increased exhaled NO in asthma is related to eosinophilic inflammation of the airways and is increased during the late response to allergen and during exacerbations and is decreased by treatment with inhaled corticosteroids[3]. As authors got increased exhaled nitric oxide in chronic bronchitis, they should have gone for sputum induction and measured eosinophils and eosinophil cationic protein (ECP) in induced sputum of the patients. Sputum induction has been advocated as a non-invasive alternative method for measuring airway inflammation with greater advantage in terms of reproducibility and simplicity. Airway inflammation in asthma is characterized by increase in activated and degranulating eosinophils in induced sputum whereas chronic bronchitis is characterized by increase in granulocyte markers of neutrophil inflammation, namely myeloperoxidase and human neutrophil lectin. Moreover, there are other indices of inflammation also like – a) hydrogen peroxide in exhaled breath condensate b) serum levels of ECP and c) urinary leukotriene E4 levels. References : 1. Delen FM, Sippei JM, Osborne ML, Law S, Thukkani N, Holden WE. Increased Exhaled Nitric Oxide in Chronic Bronchitis. Chest 2000;117:695- 701 2. Barnes PJ. Mechanisms in COPD: Differences from asthma. Chest 2000;117:10S-14S. 3. Barnes PJ, Chung KF, Page CP. Inflammatory Mediators of Asthma : An Update. Pharmacological Reviews 1998;50:515-596. |
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