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Omalizumab in the management of patients with allergic (IgE-mediated) asthma
Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
2009 (English)In: Journal of asthma and allergy, ISSN 1178-6965, Vol. 2, 49-62 p.Article in journal (Refereed) Published
Abstract [en]

Immunoglobulin E (IgE) is central to the pathophysiology of allergic asthma. Omalizumab, an anti-IgE monoclonal antibody, binds to the FcɛRI binding site on free IgE. As a result, circulating free IgE is reduced, IgE is prevented from attaching to mast cells and basophils, and FcɛRI receptor expression is down-regulated. The inflammatory response to allergens and the acute and chronic effector phases of allergic inflammation are thereby attenuated. In clinical trials in adults and adolescents, omalizumab reduced asthma exacerbations, severe asthma exacerbations, inhaled corticosteroid requirements, and emergency visits, as well as significantly improving asthma-related quality of life, morning peak expiratory flow and asthma symptom scores in patients with severe allergic (IgE-mediated) asthma. Results from clinical trials in children (<12 years) are consistent with those in the adult population. It is difficult to predict which patients will respond to omalizumab. Responders to omalizumab should be identified after a 16-week trial of therapy using the physician's overall assessment. When treatment is targeted to these responders, omalizumab provides a cost-effective therapy for inadequately controlled severe allergic (IgE-mediated) asthma. Long-term therapy with omalizumab shows the potential for disease-modification in asthma. Ongoing studies are also evaluating the use of omalizumab in other non-asthma IgE-mediated conditions.

Place, publisher, year, edition, pages
2009. Vol. 2, 49-62 p.
Keyword [en]
omalizumab, IgE, allergic asthma
National Category
Respiratory Medicine and Allergy
Identifiers
URN: urn:nbn:se:umu:diva-42591PubMedID: 21437144OAI: oai:DiVA.org:umu-42591DiVA: diva2:409796
Available from: 2011-04-11 Created: 2011-04-11 Last updated: 2011-12-21Bibliographically approved

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