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Inflammatory phenotypes in adult asthma: clinical applications

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CLINICAL RESPIRATORY JOURNAL
卷 3, 期 4, 页码 198-206

出版社

WILEY-BLACKWELL PUBLISHING, INC
DOI: 10.1111/j.1752-699X.2009.00162.x

关键词

asthma; eosinophil; noneosinophilic; phenotype; inflammation

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Background: The pattern of granulocyte infiltration can be used to identify different inflammatory phenotypes in asthma. Recognized granulocyte phenotypes using induced sputum are eosinophilic (EA), neutrophilic, mixed granulocytic and paucigranulocytic asthma. Methods: The recognition and importance of inflammatory phenotype analysis using induced sputum in adult asthma are reviewed using published literature. Results: Knowledge of inflammatory phenotype is useful because it relates to treatment response, mechanistic pathways involved in disease pathogenesis and future disease risk. The population attributable risk of asthma because of eosinophilic inflammation is about 50%, and conversely, this means that up to 50% of asthma cannot be attributed to eosinophilic inflammation, and represents asthma associated with non-eosinophilic processes. In these patients, bronchial biopsy shows significantly fewer eosinophils in the bronchial mucosa than subjects with EA. This confirms that non-eosinophilic asthma is a consistent pattern/phenotype in the airway lumen and the airway mucosa. A key aspect of asthma inflammatory phenotype analysis is that it can be applied to individual patients. The underlying principle relates to the association between a clinical response to corticosteroids and the presence of a selective sputum eosinophilia. Conclusions: Clinically useful applications of induced sputum analysis are the detection of non-adherence to corticosteroid therapy, assessment of adequacy of inhaled corticosteroid therapy, long-term therapy management in asthma, oral corticosteroid dose adjustment in refractory asthma and assessment of occupational asthma. Please cite this paper as: Gibson PG. Inflammatory phenotypes in adult asthma: clinical applications. The Clinical Respiratory Journal 2009; 3: 198-206.

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