|Ewa Cichocka-Jarosz, Ewa Nizankowska-Mogilnicka*|
Klinika Chorób Dzieci Katedry Pediatrii Collegium Medicum UJ, ul. Wielicka 265, 30-663 Kraków
*Klinika Pulmonologii II Katedry Chorób Wewnętrznych Collegium Medicum UJ, ul. Skawińska 8, 31-066 Kraków
Atopy – an inherited, genetically determined capacity to produce abnormal amounts of specific IgE – is the basic cause of the so-called atopic diseases – bronchial asthma, allergic rhinitis and allergic conjunctivitis. Immunoglobulin E expresses biological action through specific high affinity (FceRI) and low affinity (FceRII) receptors, presented on the surface of different cells. The regulation of IgE synthesis is controlled by T-lymphocytes. Due to the growing prevalence of atopic diseases, the new methods of causal treatment, apart from traditional ones, are explored. Up till now the only method influencing the immunological patomechanism of atopic diseases was specific immunotherapy. The new alternative may be the humanized murine monoclonal antibody anti-IgE (omalizumab, rhuMAb-E25). The drug binds to free IgE, reduces its level, blocks the binding of IgE to FceRI receptor and downregulates the activation of inflammatory cells. First attempts at applying omalizumab in randomized double blind studies, indicate its efficacy both in adults and children with bronchial asthma or allergic rhinitis. The usefulness of the drug is associated with the improvement of clinical symptoms score, lung function tests and the quality of life, reduction of rescue medication, steroid-sparing effect. The drug is well tolerated, with side-effects similar to those of placebo. This novel promising therapy requires further follow-up monitoring as far as its efficacy and safety are concerned, giving the hope for widening the indications for its application.
Alergia Astma Immunologia, 2002, 8(2), 65-72
keywords: IgE, atopia, omalizumab, rhuMAb-E25, IgE, atopy, omalizumab, rhuMAb-E25
pages: from 65 to 72
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