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Available from: Annick Lim, Jul 27, 2015
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    • "It was reported that both STAT3 mutation-positive and STAT3 mutation-negative HIES exhibited a profound deficit in TH17 differentiation [63]. Several studies reported clinical improvement in patients with severe atopic eczema with high serum IgE level [63–65]. "
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    ABSTRACT: Omalizumab, a humanized mAb that binds to the CH3 domain near the binding site for the high-affinity type-I IgE Fc receptors of human IgE, can neutralize free IgE and inhibit the IgE allergic pathway without sensitizing mast cells and basophils. We found that omalizumab in patients with severe persistent asthma (SPA) was an effective therapy for asthma and the following co-morbid conditions: chronic urticaria (CU), bee venom allergy, latex allergy, atopic dermatitis, food allergy and Samter’s syndrome. Information on the use of omalizumab in treatment of asthma and other allergic diseases has improved our understanding that treatment acts on many levels, including regulating levels of inflammatory proteins, including cytokines (copper-containing alpha- 2-glycoprotein, total antioxidant capacity, MDA, NO, H2O2, CXCL8, IL-10, TGF-β, GMCSF, IL-17, IL-1β), MPV, Hs-CRP, eosinophil cationic peptide, vitamin-D (25(OH)D), homocysteine (Hcy), OX-2, d- dimer, albumin, and sApo-2L. The decrease in Hcy concentrations and increase in 25(OH)D also support the existence of a vascular endothelial protection mechanism. Mediators and cells classically involved in pro-coagulant and anticoagulant pathways together play a role in SPA and CU pathophysiology and omalizumab effect. The mechanism of action of omalizumab in the treatment of asthma is believed to be multifactorial, and includes effects mediated through altered production of redox metabolites, extrinsic coagulation pathway, oxidative markers-related mi RNA, TRAIL-related mi RNA, and regulation of production of known inflammatory proteins.
    Medical science monitor: international medical journal of experimental and clinical research 06/2014; 20. DOI:10.12659/MSM.890137 · 1.43 Impact Factor
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    • "Of note, the present improvement of QoL scores in patients with concomitant atopic dermatitis and asthma was observed with low-dose anti IgE treatment (233 ± 109 mg/2 weeks) and, therefore, was in a much lower dosage than required for the complete removal of IgE from the circulation, as recently also described by Lim and Belloni [1,10]. They had observed free IgE remained basically stable over the omalizumab treatment period and suggested other, molecular effects such as a switch to reduced IgE mRNA production responsible for skin improvement [1,10]. "
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    ABSTRACT: Anti IgE treatment with omalizumab is efficacious in the treatment of patients suffering from allergic asthma, improving asthma control and improving quality of life. Furthermore, this approach could be beneficial for patients with concomitant atopic dermatitis. We assessed quality of life and asthma control in atopic patients with allergic asthma and concomitant atopic dermatitis versus those with asthma and without atopic dermatitis treated with omalizumab. - A total of 22 patients with severe allergic asthma were treated with omalizumab for 12 months. 13 patients with allergic asthma without concomitant atopic dermatitis (IgE 212 ± 224 IU/ml) and 9 patients with concomitant allergic asthma and atopic dermatitis (IgE 3,528 ± 2,723 IU/ml) were included. Asthma-related quality of life (AQLQ), atopic dermatitis related quality of life (DLQI), and asthma-related treatment were compared between both groups at baseline and after initiating omalizumab treatment. - DLQI was significantly in favor of omalizumab after 2 months in the atopic dermatitis/asthma group (P = 0.01); AQLQ was improved after 6 months in the asthma group (P = 0.01), while no change was seen in AQLQ in the atopic dermatitis/asthma group (P = 0.12). Omalizumab controlled oral corticosteroid use more effective (P<0.01) in patients with asthma and atopic dermatitis (in 9/9 cases) compared to patients with asthma alone (9/13). Baseline IgE as well as other factors do not predict response to omalizumab. - Omalizumab is effective in improving atopic dermatitis-related quality of life scores and modulates oral corticosteroid use in patients with concomitant asthma and atopic dermatitis in a positive fashion.
    European journal of medical research 09/2011; 16(9):407-10. DOI:10.1186/2047-783X-16-9-407 · 1.50 Impact Factor
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    • "Six patients responded with satisfying to very good clinical response based on scoring (Scoring Atopic Dermatitis [SCORAD]). On the other hand, 5 patients showed either no relevant changes or clinical deterioration at the conclusion of the study (10 cycles of treatment) [66]. On the basis of the limited data available, the role for omalizumab in the treatment of atopic dermatitis requires further investigation. "
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    ABSTRACT: The importance of immunoglobulin E (IgE) in atopic disorders such as asthma, allergic rhinitis, food allergies, and atopic dermatitis is well established. Elevation of total serum IgE is typically found in many atopic patients, and in predisposed individuals, allergen-specific IgE is produced. The availability of humanized monoclonal antibodies against IgE has provided a new therapeutic option and tool to explore the role IgE in allergic diseases and the effects of inhibiting IgE itself. Omalizumab is a humanized, monoclonal antibody that recognizes and binds to the Fc portion of the IgE molecule. Administration of omalizumab results in a rapid and substantial decrease in free IgE in serum. Consequently, the activity of cell populations involved in allergic inflammation, including mast cells, eosinophils, basophils, and antigen-presenting cells, is affected as well. Clinically, anti-IgE therapy has already been proven to be useful in the treatment of asthma and allergic rhinitis. The aim of this review is to provide an overview of the mechanisms of action of anti-IgE therapy as well as its efficacy in the treatment of allergic diseases, especially asthma. Considerations regarding dosing and safety of omalizumab will be addressed as well.
    World Allergy Organization Journal 10/2008; 1(10):174-83. DOI:10.1097/WOX.0b013e318187a310
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