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      The Pathophysiology, Diagnosis and Treatment of Allergic Rhinitis

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          Abstract

          Treatment of AR requires a stepwise approach depending on the severity and duration of symptoms. Treatment options for AR consist of allergen avoidance, pharmacotherapy, immunotherapy and surgery. For the mechanisms of AR, anti-IgE antibody and specific antibody to cytokines such as IL-4 or IL-5 that correlate with allergic inflammation have recently emerged. SLIT is currently widely used due to its efficacy, safety and convenience, which replaces subcutaneous immunotherapy. Although allergen avoidance and immunotherapy are theoretically ideal, antihistamines and intranasal corticosteroids will play the main role in the management of AR until an innovative treatment develops. However, patients' main symptom, the duration and severity of AR, patients' compliance, safety of medication and cost-effectiveness should be considered when treatment options are chosen. In conclusion, physicians should be aware of etiology, pathophysiology, symptoms, signs and diseases related to AR in order to make a correct diagnosis and choose a proper treatment option for each patient.

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          Most cited references85

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          Advances in H1-antihistamines.

          F Simons (2004)
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            The anti-inflammatory effects of omalizumab confirm the central role of IgE in allergic inflammation.

            Anti-IgE therapy with omalizumab reduces serum levels of free IgE and downregulates expression of IgE receptors (Fc epsilonRI) on mast cells and basophils. In the airways of patients with mild allergic asthma, omalizumab reduces Fc epsilonRI+ and IgE+ cells and causes a profound reduction in tissue eosinophilia, together with reductions in submucosal T-cell and B-cell numbers. In patients with seasonal allergic rhinitis, omalizumab inhibits the allergen-induced seasonal increases in circulating and tissue eosinophils. Omalizumab decreases Fc epsilonRI expression on circulating dendritic cells, which might lead to a reduction in allergen presentation, T(H)2 cell activation, and proliferation. As a systemic anti-IgE agent, omalizumab has demonstrated clinical efficacy in patients with moderate and severe allergic asthma and in those with seasonal and perennial allergic rhinitis, as well as in patients with concomitant allergic asthma and allergic rhinitis. The anti-inflammatory effects of omalizumab at different sites of allergic inflammation and the clinical benefits of anti-IgE therapy in patients with allergic asthma and allergic rhinitis emphasize the fundamental importance of IgE in allergic inflammation.
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              Omalizumab-induced reductions in mast cell Fce psilon RI expression and function.

              By design, omalizumab binds free IgE in the circulation and prevents its attachment to the surface of mast cells and basophils, thereby preventing them from responding to allergens. Previously, omalizumab rapidly reduced free IgE levels, as well as basophil high-affinity IgE receptors, leading to significant reductions in basophil mediator response to allergen. It is assumed that tissue mast cells are similarly altered in their Fc epsilon RI density and function. We examined the phenotypic shift of skin mast cells in parallel to that of blood basophils in 3 subjects infused with omalizumab. Three subjects with allergic rhinitis underwent intradermal skin test titration with house dust mite antigen at days 0, 7, 70, and 196 of omalizumab treatment. As control subjects, 5 untreated subjects with allergic rhinitis were evaluated at similar time points. All subjects underwent skin biopsy 18 to 24 hours later at the site of allergen injection. Biopsy specimens were characterized by means of immunohistochemisty for tryptase and Fc epsilon RI alpha immunoreactivity, as well other markers (CD3, CD45RO, CD68, cutaneous lymphocyte antigen, and major basic protein). Omalizumab recipients, but not control subjects, demonstrated reductions in Fc epsilon RI alpha immunoreactivity at days 70 and 196 in parallel with reductions in the acute wheal response to allergen. However, no reductions in tryptase-positive cells were noted at these time points. Reductions in free IgE levels by omalizumab leads to a rapid reduction in basophil Fc epsilon RI receptor expression. In contrast, the time course for the decrease of Fc epsilon RI expression in skin mast cells is slower and associated with decreased acute allergen wheal size.
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                Author and article information

                Journal
                Allergy Asthma Immunol Res
                AAIR
                Allergy, Asthma & Immunology Research
                The Korean Academy of Asthma, Allergy and Clinical Immunology; The Korean Academy of Pediatric Allergy and Respiratory Disease
                2092-7355
                2092-7363
                April 2010
                24 March 2010
                : 2
                : 2
                : 65-76
                Affiliations
                Department of Otorhinolaryngology, Seoul National University College of Medicine, Seoul, Korea.
                Author notes
                Correspondence to: Yang-Gi Min, MD, PhD, Department of Otorhinolaryngology, Seoul National University College of Medicine, 101 Daehak-ro, Jongno-gu, Seoul 110-744, Korea. Tel: +82-2-760-2446; Fax: +82-2-745-2387; ygmin312@ 123456dreamwiz.com
                Article
                10.4168/aair.2010.2.2.65
                2846743
                20358020
                f16a281d-eba7-40ae-8257-a17f63d13258
                Copyright © 2010 The Korean Academy of Asthma, Allergy and Clinical Immunology • The Korean Academy of Pediatric Allergy and Respiratory Disease

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 01 March 2010
                : 04 March 2010
                Categories
                Review

                Immunology
                therapy,physiopathology,seasonal allergic rhinitis,hypersensitivity,perennial allergic rhinitis,diagnosis

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