Abstract

The causal role of immunoglobulin E (IgE) in triggering the cascade of biochemical events leading to allergic disease is well established. Treatments that selectively inhibit IgE activity are a logical approach in managing the allergic response. Omalizumab is a recombinant humanised monoclonal antibody which specifically binds to the Cε3 domain of immunoglobulin (Ig) E, the site of high-affinity IgE receptor binding. The clinical benefit and steroid-sparing effect of treatment with the anti-immunoglobulin-E (IgE) antibody, Omalizumab, was assessed in patients with moderate-to-severe allergic asthma and seasonal allergic rhinitis. Intravenous and subcutaneous administration of anti-IgE mAb reduces circulating levels of IgE in atopic patients to low levels commonly seen in non-atopic individuals. Anti-IgE therapy offers protection against allergen-induced bronchoconstriction, reduces the need for short acting inhaled beta 2-agonist and corticosteroids among asthmatic patients and reduces severity of symptoms of allergic rhinitis. Adverse events were infrequent in clinical trials of omalizumab, and not significantly different from placebo. The most frequent drug-related event was mild to moderate urticaria. They do not induce anaphylaxis and the occurrence of antibodies against anti-IgE mAb is sporadic. The results of cited studies suggest that humanized anti-IgE monoclonal antibodies may have important immunotherapeutic benefit for treatment of allergic disorders.

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