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P159 The use of omalizumab in severe asthma is associated with a decline in blood eosinophils
  1. LJ Holmes1,
  2. G Tavernier2,
  3. S Fowler2,
  4. K Hince1,
  5. RM Niven2
  1. 1University Hospital of South Manchester, Manchester, UK
  2. 2Institute of Inflammation and Repair, Manchester Academic Health Sciences Centre, University of Manchester and National Institute of Health Research Respiratory and Allergy Clinical Research Facility, University Hospital of South Manchester, Manchester, UK

Abstract

Introduction/aim Omalizumab (Xolair) is a recombinant humanised monoclonal antibody licensed for the treatment of severe allergic asthma patients with IgE mediated disease. The mechanism of action of omalizumab is to bind to IgE preventing interaction with FCERI (high affinity receptors) upon the surface of mast cells and basophils, thereby reducing the activation of the inflammatory cascade and associated clinical symptoms. Although blood eosinophilia is a useful measure of airway inflammation, the correlation between blood eosinophils and omalizumab treatment has not been described outside clinical trial. Therefore, our aims were to identify whether the introduction of omalizumab is associated with a change in the blood eosinophil count within our cohort of patients with severe asthma.

Methods We collected measurements of blood eosinophils in patients maintained on omalizumab for periods 12 months pre and post, and (where available) 24 months pre and post initiation of therapy. We also investigated any correlation between blood eosinophils pre and post treatment versus clinical parameters including total IgE and omalizumab dose.

Results Complete data sets including 12-month blood eosinophil data were available for 49 of our current cohort of 92 patients on treatment. The mean blood eosinophil count dropped from 0.33 × 109cells/l (IQR 0.37) × 109cells/l pre-treatment to 0.22 × 109cells/l (IQR 0.30) post treatment (p = <0.001).

Additionally, we widened the window to 24 months pre and post initiation of treatment, if blood eosinophil data was not available at 12 months. Data for 59 patients demonstrated similar significant reduction in mean blood eosinophil, 0.34 × 109cells/l (IQR 0.34) pre-treatment to 0.23 × 109cells/l (IQR 0.29) ( p = 0 .003).

No association was seen between the changes in mean blood eosinophil counts post treatment versus total monthly omalizumab dose and baseline total IgE.

Conclusion Our data demonstrates a significant reduction in blood eosinophils in patients who are receiving omalizumab treatment when comparing blood eosinophils at 12 and 24 months pre and post treatment. Future work should investigate whether this is a direct result of omalizumab therapy, due to confounding by other treatment, or a marker of improved asthma control.

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