Journal of Allergy & Therapy

Omalizumab for Treatment of Idiopathic Angioedema

Breschi Schwartz^* Department of Allergy and Immune Diseases, Yale University, New Haven, United States
^*Correspondence: Breschi Schwartz, Department of Allergy and Immune Diseases, Yale University, New Haven, United States, Email:

Received: 04-Jul-2022, Manuscript No. JAT-22-17740 ; Editor assigned: 07-Jul-2022, Pre QC No. JAT-22-17740 (PQ); Reviewed: 22-Jul-2022, QC No. JAT-22-17740 ; Revised: 01-Aug-2022, Manuscript No. JAT-22-17740 (R); Published: 08-Aug-2022, DOI: 10.35248/2155-6121.22.13.296

Description

Angioedema (AE) is characterised by recurring episodes of transitory swelling involving the submucosa or deep dermis, frequently impacting the skin and respiratory tissues. Based on aetiology and mechanism, AE can be broadly divided into three classes. These include idiopathic, mast cell-mediated, and bradykinin-mediated. Mast cell mediated processes can manifest as solitary angioedema without urticaria but are typically accompanied with urticaria due to either an IgE mediated reaction or direct mast cell activation.

Bradykinin-mediated mechanisms, such as those related to Angiotensin-Converting Enzyme Inhibitors (ACE-I), DPP4 inhibitors, or hereditary angioedema caused by C1 inhibitor deficiency, dysfunction, or other recognised genetic variants associated with hereditary angioedema with normal C1 inhibitor level and function, are not related to urticaria. Bradykininmediated mechanisms involve an overproduction of bradykinin or the inhibition of its degradation. Idiopathic Angioedema (IAE) is the term used to describe bouts of angioedema without urticaria for which no cause has been identified despite extensive research. IAE is occasionally used to describe patients while additional testing is being done, so this word does not necessarily indicate to a specific condition but rather a diagnostic problem in which the cause of edoema has not yet been identified.

H2-antihistamines, leukotriene-receptor antagonists, systemic glucocorticoids, cyclosporine, hydroxychloroquine, dapsone, methotrexate, sulfasalazine, and intravenous immune globulin are among the treatment choices for people who do not respond to H1-antihistamines. Until yet, none of these medications have been given regulatory approval to treat chronic idiopathic urticaria. Additionally, there is a lack of evidence to support the use of these medications, and prolonged use of some of the pharmaceuticals may result in serious side effects. A recombinant humanised IgG1 monoclonal antibody known as omalizumab selectively binds to free IgE, inhibits it from binding to the high-affinity IgE receptor (FcRI), and decreases the density of FcRI on the surface of mast cells, basophils, and dendritic cells. It received FDA approval in 2014 for individuals with Chronic Spontaneous Urticaria (CSU) who continue to experience symptoms despite H1 antagonist medication due to evidence that it significantly improves outcomes in both patients with and without AE. Data from the initial phase 3 trials, which comprised roughly 975 individuals with CSU (of whom 41%-53% also experienced AE), as well as other recently published findings, interestingly showed improvement in AE symptoms as well.

The effective use of omalizumab in a group of three IAE patients was initially reported in 2007. There are currently no prospective randomised trials for omalizumab treatment of IAE. As a result, we suggested that omalizumab-based anti-IgE therapy would be advantageous for IAE patients. In this patient population, the effects of omalizumab started to manifest a week after treatment began. In comparison to the placebo group, the median time to MID response in the weekly itch-severity score was substantially shorter in the 300 mg and 150 mg omalizumab groups (1 week and 2 weeks, respectively) than in the placebo group (4 weeks). Additionally, the phase 2 trials revealed that the UAS and decreased within the first week of omalizumab treatment.