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• W2116095013 abstract "The definition of asthma has changed from that of a clinical disease (wheeze and/or cough in a setting where asthma is likely and other, rarer conditions have been excluded) (1) to a combination of clinical symptoms and pathology, usually describing airway inflammation (2). The concept of including inflammation in the definition has been questioned (3). In young children it is impractical to include inflammation as a requirement for the diagnosis. We know that a large part of the asthma phenotype in young adults at least is related to helper T type 2 (Th2) lymphocyteand eosinophil-mediated airway inflammation, but even in atopic adult asthma other important mechanisms may be involved (4, 5). These may include noneosinophilic inflammation (neutrophils or other cells, chemical mediators acting directly on the airway, neurogenic inflammation, plasma extravasation) and the effect of a possible reduction in baseline airway caliber, either for developmental reasons or secondary to acquired remodeling (6). In the context of other childhood wheezing illness, both bronchoscopic (7) and blind (8) lavage studies suggest that pure virus-associated wheeze is not an eosinophilic disease and is not even due to or associated with chronic airway inflammation. Other evidence suggests that the eosinophil may not always be the main cell involved in airway inflammation. The neutrophil is an important component of the late-phase response (9) and of endotoxin-induced asthma (10). Furthermore, a subgroup of patients with asthma without elevated sputum eosinophil levels and who were poorly responsive to corticosteroids has been described (11). Finally, there may be significant differences in the pathology of severe and mild to moderate asthma (12). We also know that the treatment with inhaled or oral corticosteroids of what is presumed to be airway inflammation in children reduces blood markers of T cell activation and cytokine levels (13) and reduces sputum eosinophilia (14) and nitric oxide (NO) levels (15). This suggests that antiinflammatory treatment reduces some forms of airway inflammation. There is a poor correlation between these markers when they are used to measure the response to antiinflammatory therapy (16). Uncontrolled trials in children (17) and controlled studies in adults (18) indicate that a delay in the initiation of inhaled corticosteroid therapy for the treatment of chronic asthma results in poorer long-term lung function. This suggests that untreated inflammation leads to secondary airway remodeling, which becomes irreversible. However, there are few data on the relationship between early inflammatory processes and structural changes in the airways of patients with asthma. We also know that corticosteroids are not disease modifying in chronic childhood asthma, at least when started at the conventional time. Even after 2 yr, the plateau for bronchial hyperreactivity is not reached and relapse occurs if treatment is stopped (19)." @default.
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• W2116095013 date "2000-08-01" @default.
• W2116095013 modified "2023-10-12" @default.
• W2116095013 title "Clinical Implications of Inflammation in Young Children" @default.
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• W2116095013 doi "https://doi.org/10.1164/ajrccm.162.supplement_1.maic-3" @default.
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