Skip to main content
Article thumbnail
Location of Repository

Subclinical phenotypes of asthma

By Peter Bradding and Ruth H. Green

Abstract

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.0b013e32833489a9Purpose 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.\ud \ud 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.\ud \ud Summary: The detailed phenotyping of asthma will allow the successful targeting of existing and novel therapies to those patients most likely to gain benefit

Publisher: Lippincott Williams & Wilkins
Year: 2010
DOI identifier: 10.1097/ACI.0b013e32833489a9
OAI identifier: oai:lra.le.ac.uk:2381/8013
Journal:

Suggested articles

Citations

  1. (2007). A study to evaluate safety and efficacy of Mepolizumab in patients with moderate persistent asthma. Am J Respir Crit Care Med doi
  2. (2003). Anti-IL-5 treatment reduces deposition of ECM proteins in the bronchial subepithelial basement membrane of mild atopic asthmatics. doi
  3. (2008). Clarithromycin targets neutrophilic airway inflammation in refractory asthma. doi
  4. (2008). Cluster analysis and clinical asthma phenotypes. doi
  5. (2006). Cytokines or Their Antagonists for the Treatment of Asthma. Chest doi
  6. (2003). Effect of SCH55700, a humanized antihuman interleukin-5 antibody, in severe persistent asthma: a pilot study. Am J Respir Crit Care Med doi
  7. (2000). Effects of an interleukin-5 blocking monoclonal antibody on eosinophils, airway hyper-responsiveness, and the late asthmatic response. Lancet doi
  8. (2009). Eosinophils in asthma--closing the loop or opening the door? doi
  9. (2001). Heterogeneity of airway inflammation in persistent asthma : evidence of neutrophilic inflammation and increased sputum interleukin-8. Chest doi
  10. (2008). Increased sputum and bronchial biopsy IL-13 expression in severe asthma. doi
  11. Mepolizumab in refractory eosinophilic asthma. Thorax 2009,in press. Patients who respond best to anti-IL-5 therapy have a poor bronchodilator response to 2-agonists.
  12. (1994). Role of interleukin-8 (IL-8) and an inhibitory effect of erythromycin on IL-8 release in the airways of patients with chronic airway diseases. Infect Immun
  13. (2007). The reclassification of asthma based on subphenotypes. Curr Opin Allergy Clin Immunol doi

To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.