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Anti-IgE Therapy with Omalizumab Decreases Endothelin-1 in Exhaled Breath Condensate of Patients with Severe Persistent Allergic Asthma.

Authors: Zietkowski, Z  Skiepko, R  Tomasiak-Lozowska, MM  Bodzenta-Lukaszyk, A 
Citation: Zietkowski Z, etal., Respiration. 2010 Jun 26.
Pubmed: (View Article at PubMed) PMID:20588001
DOI: Full-text: DOI:10.1159/000317137

Background: Omalizumab is a humanized monoclonal anti-IgE antibody, especially useful for the treatment of severe persistent allergic asthma, inadequately controlled despite regular therapy. Objectives: The aim of the study was to determine the effect of omalizumab treatment on changes in endothelin-1 (ET-1), which plays an important role in the development of airway inflammation and remodeling in exhaled breath condensate (EBC) in patients with severe asthma. Methods: The study was conducted in a group of 19 patients with severe persistent allergic asthma treated with conventional therapy (according to the Global Initiative for Asthma, 2006) and with or without omalizumab (9 vs. 10 patients). Changes in ET-1 in EBC compared with other inflammatory parameters [exhaled nitric oxide - (FE(NO)), blood eosinophil count, and serum eosinophil cationic protein (ECP)] were measured after 16 and 52 weeks of therapy. Results: Omalizumab-treated patients demonstrated a statistically significant decrease in the concentrations of ET-1 in EBC, FE(NO), serum ECP, and blood eosinophil count and an increase in spirometry parameters compared to patients with conventional therapy. In the group of omalizumab-treated patients, statistically significant correlations between the decrease in ET-1 in EBC and a decrease in FE(NO), ECP, and blood eosinophil count as well as the increase in forced expiratory volume in 1 s after omalizumab therapy were revealed. Conclusions: Our results confirmed that anti-IgE therapy with omalizumab in patients with severe persistent allergic asthma results in decreased expression of ET-1 in the airways. This could be very important in limiting airway inflammation and bronchial structural changes caused by such treatment in asthmatic patients.


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CRRD Object Information
CRRD ID: 4144895
Created: 2010-10-21
Species: All species
Last Modified: 2010-10-21
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.