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Subclinical phenotypes of asthma

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journal contribution
posted on 2010-06-07, 15:52 authored by Peter Bradding, Ruth H. Green
Purpose of review: Asthma is a heterogeneous disease. Identification of specific subphenotypes of asthma may further our understanding of pathophysiology and treatment response, leading to the better targeting of both existing and novel antiasthma therapies. An accurate and comprehensive clinicopathological classification system therefore remains an important priority for asthma research. The present review discusses the important recent literature in this field. Recent findings: Cluster analysis in patients with severe asthma has suggested the presence of four distinct clinical phenotypes, two with eosinophilic airway inflammation, and two without. Patients with eosinophilic inflammation benefit most from a management strategy targeting the sputum eosinophil count. Molecular phenotying utilizing gene arrays in steroid-naive asthmatic individuals reveals two distinct subgroups (Th2-high and Th2-low) based on the expression of Th2 cytokine genes (IL-5, IL-13) and Th2-responsive genes. The Th2-high group exhibit clinical features typical of patients with eosinophilic disease. Targeting anti-IL-5 therapy to patients with evidence of eosinophilic airway inflammation and recurrent asthma exacerbations markedly reduces the asthma exacerbation rate, but day-to-day asthma symptoms remain unchanged. Summary: The detailed phenotyping of asthma will allow the successful targeting of existing and novel therapies to those patients most likely to gain benefit.

History

Citation

Current Opinion in Allergy and Clinical Immunology, 2010, 10 (1), pp. 54-59.

Published in

Current Opinion in Allergy and Clinical Immunology

Publisher

Lippincott Williams & Wilkins

issn

1528-4050

Available date

2010-06-07

Publisher version

http://ovidsp.tx.ovid.com/sp-3.17.0a/ovidweb.cgi?QS2=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

Notes

This is the author's final draft of the paper published as Current Opinion in Allergy and Clinical Immunology, 2010, 10 (1), pp. 54-59. The final version is available from http://journals.lww.com/co-allergy/pages/articleviewer.aspx?year=2010&issue=02000&article=00010&type=abstract. Doi: 10.1097/ACI.0b013e32833489a9

Language

en

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