Methods: We reported that Omalizumab in patients with severe persistent asthma (SPA) was an effective therapy for asthma and co-morbid conditions (chronic urticaria (CU), bee venom allergy, latex allergy, bullous pemphigoid, atopic dermatitis, food allergy, Samters syndrome, diabetes mellitus, cardiovascular conditions).
Results:
Our knowledge concerning 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 (MDA, NO, H2O2, CXCL8, IL-10, TGF-β, GCSF, IL-17, IL-1β), PT, PTT, INR, MPV, platelet count, Hs-CRP, eosinophil cationic peptide, vitamin-D (25(OH)D), homocystein (Hcy) , OX-2, d- dimer , albumin and sApo-2L. The decrease in Hcy concentrations and increase in 25(OH)D also support the possible vascular endothelial protection mechanism. Mediators and cells classically involved in pro-coagulant and anticoagulant pathways altogether play a role in SPA and CU pathophysiology and Omalizumab effect.
Conclusions: Since Omalizumab reduces the expression of FcεRI on circulating basophils and mast cells, it seems to lower the activity potentials of basophils and mast cells, thereby reducing the potential reactivity of these cells .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, Oxidative markers related mi RNA, TRAIL related mi RNA, and regulation of production of known inflammatory proteins.