Omalizumab reduces bronchial mucosal IgE and improves lung function in non-atopic asthma.
Omalizumab therapy of non-atopic asthmatics reduces bronchial mucosal IgE and inflammation and preserves/improves lung function when disease is destabilised by staged withdrawal of therapy.18 symptomatic, non-atopic asthmatics were randomised (1:1) to receive omalizumab or identical placebo treatment in addition to existing therapy for 20 weeks. Bronchial biopsies were collected before and after 12-14 weeks of treatment, then the patients destabilised by substantial, supervised reduction of their regular therapy. Primary outcome measures were changes in bronchial mucosal IgE+cells at 12-14 weeks, prior to regular therapy reduction, and changes in lung function (forced expiratory volume in 1 s) after destabilisation at 20 weeks. Quality of life was also monitored.Omalizumab but not placebo therapy significantly reduced median total bronchial mucosal IgE+cells (p<0.01) but did not significantly alter median total mast cells, plasma cells, B lymphocytes, eosinophils and plasmablasts, although the latter were difficult to enumerate, being distributed as disperse clusters. By 20 weeks, lung function declined in the placebo-treated patients but improved in the omalizumab treated patients, with significant differences in absolute (p=0.04) and % predicted forced expiratory volume in 1 s (p=0.015).Omalizumab therapy of non-atopic asthmatics reduces bronchial mucosal IgE+mast cells and improves lung function despite withdrawal of conventional therapy.
Dept of Respiratory Medicine and Allergy, and Randall Division of Cell and Molecular Biophysics, King's College London, London, UK prathap.pillai@kcl.ac.uk.
Prathap
P
Pillai
Dept of Respiratory Medicine and Allergy, and Randall Division of Cell and Molecular Biophysics, King's College London, London, UK.
Yih-Chih
YC
Chan
Dept of Respiratory Medicine and Allergy, and Randall Division of Cell and Molecular Biophysics, King's College London, London, UK.
Shih-Ying
SY
Wu
Dept of Respiratory Medicine and Allergy, and Randall Division of Cell and Molecular Biophysics, King's College London, London, UK.
Line
L
Ohm-Laursen
Dept of Respiratory Medicine and Allergy, and Randall Division of Cell and Molecular Biophysics, King's College London, London, UK.
Clare
C
Thomas
Section for Allergy and Clinical Immunology at NHLI, Imperial College London, London, UK.
Stephen R
SR
Durham
Section for Allergy and Clinical Immunology at NHLI, Imperial College London, London, UK.
Andrew
A
Menzies-Gow
Dept of Respiratory Medicine and Allergy, Homerton University Hospital NHS Foundation Trust, London, UK.
Raj K
RK
Rajakulasingam
Dept of Respiratory Medicine and Allergy, and Randall Division of Cell and Molecular Biophysics, King's College London, London, UK.
Sun
S
Ying
Dept of Respiratory Medicine and Allergy, and Randall Division of Cell and Molecular Biophysics, King's College London, London, UK.
Hannah J
HJ
Gould
Dept of Respiratory Medicine and Allergy, and Randall Division of Cell and Molecular Biophysics, King's College London, London, UK.
Chris J
CJ
Corrigan
D000328:Adult; D000368:Aged; D018927:Anti-Asthmatic Agents / Q000627:therapeutic use*; D001249:Asthma / Q000188:drug therapy*; D001980:Bronchi / Q000473:pathology*; D001999:Bronchoscopy; D004311:Double-Blind Method; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood*; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D000069444:Omalizumab / Q000627:therapeutic use*; D000075082:Proof of Concept Study; D011788:Quality of Life; D016896:Treatment Outcome; D006113:United Kingdom; D055815:Young Adult
D018927:Anti-Asthmatic Agents; D000069444:Omalizumab; D007073:Immunoglobulin E