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Author: Anoma Ranaweera, Medical Writer, Auckland, New Zealand. DermNet Chief Editor in Chief: Adjunct A/Prof Dr Amanda Oakley, Dermatologist, Hamilton, New Zealand. First published December 2013; updated April 2020. Copy edited by Gus Mitchell/Maria McGivern.
Omalizumab is a humanised monoclonal antibody that binds to circulating immunoglobulin E (IgE) and reduces the release of inflammatory mediators from mast cells and basophils.
In New Zealand, it is currently (as of 2020) licensed as an add-on therapy for patients with severe, persistent allergic asthma and for patients 12 years of age or older with severe chronic idiopathic (spontaneous) urticaria that remain symptomatic despite H1-antihistamine treatment. It is funded in New Zealand by PHARMAC on Special Authority application under certain circumstances .
It is given by subcutaneous injection once every 4 weeks.
The trade name of omalizumab is Xolair™.
Chronic spontaneous urticaria (also called chronic idiopathic urticaria) is defined as hives or weals that last for at least 6 weeks, with or without angioedema. Urticaria is often extremely itchy, interfering with sleep, daily activities, social interactions, school, and work life.
Symptoms may resolve after a few months; however in about 50% of cases symptoms persist for 3–5 years, and in 20% of cases symptoms can persist for more than 10 years.
Urticaria most often results from the effect of histamine on H1-receptors located on the endothelial cells lining blood vessels. Histamine causes the cells to separate, so that tissue fluid leaks out, forming a weal. Histamine also affects sensory nerves, resulting in a neurogenic erythematous flare and pruritus [2,3].
Chronic urticaria may be refractory to antihistamines and associated with a pronounced cellular infiltrate.
Omalizumab is intended to be used as second-line therapy for the treatment of chronic spontaneous urticaria that is refractory to oral antihistamines. Many patients also fail to respond to a variety of other systemic therapies including systemic steroids and immunomodulating drugs.
Immunoglobulin E (IgE) triggers an allergic reaction (eg, asthma) in response to an allergen (eg, cat dander). Although chronic spontaneous urticaria is not due to allergy, it occurs through a similar pathway.
Omalizumab has been designed to recognise and attach to a specific structure on circulating human IgE. This prevents IgE binding to high-affinity receptors (FcεRI) on the surface of mast cells and basophils, thus reducing receptor expression and the release of inflammatory mediators .
Results of three Phase III trials (ASTERIA I, ASTERIA II, and GLACIAL) support the efficacy of omalizumab in chronic spontaneous urticaria.
|Omalizumab 300 mg||-9.8||< 0.001|
|Omalizumab 150 mg||-8.1||= 0.001|
|Omalizumab 75 mg||-5.9||= 0.46|
The X‐ACT study aimed to examine the effect of omalizumab treatment on quality of life (QoL) in chronic spontaneous urticaria (CSU) patients with angioedema refractory to high doses of H1‐antihistamines .
In this phase III double-blind randomised study patients were randomised 1:1 to receive omalizumab 300 mg SC or placebo every 4 weeks for 28 weeks. 68 patients (omalizumab, n = 35; placebo, n = 33) completed the 28‐week treatment period. All were chronic spontaneous urticaria patients (18–75 years) with ≥4 angioedema episodes during the 6 months before inclusion.
Angioedema‐related quality of life (QoL), skin‐related QoL impairment, and psychological well‐being were assessed.
At baseline, the mean (SD) total Angioedema QoL (AE‐QoL; 56.2 [18.7] and 59.9 [19.2]) and Dermatology Life Quality Index (DLQI; 14.6 [5.7] and 16.6 [7.3]) score were high in the omalizumab and placebo groups, respectively.
Following omalizumab treatment initiation, the mean angioedema activity scores (AAS7; consisting of an opening question [Have you had a swelling episode in the last 24 h?], followed by the five specific AAS questions to determine the severity and impact of the angioedema episode, decreased rapidly with significant differences observed as early as week 4 through to week 28.
The mean (SD) AAS7 scores increased to placebo levels (omalizumab, 10.2 [19.6]; placebo, 9.8 [12.0]) after discontinuation of omalizumab at Week 36.
The most severely affected subdomains of the AE‐QoL were fears/shame, fatigue/mood, and functioning. The most severely affected subdomains of the DLQI score included daily activities and leisure.
General psychological and well-being improved with omalizumab treatment. In the omalizumab group, the mean (SD) WHO‐5 score [The World Health Organisation -5 Well-Being Index) was 10.0 (5.5) at baseline and increased above the depression threshold to 18.6 (5.1) by the end of the treatment period. The corresponding results in the placebo group were 7.7 (5.3) at baseline and 11.5 (5.8) at week 28 (least square mean difference between groups at week 28, P < 0.001).
So far, there is no evidence that omalizumab is disease-modifying. When patients stopped the study drug, their symptoms recurred. At the end of 16 weeks off treatment, symptoms of urticaria were similar to patients treated with placebo. When omalizumab was restarted in patients that had previously responded, the omalizumab was again effective.
Chronic inducible urticaria, such as solar urticaria or cold urticaria, does not always respond well to antihistamines. To date, no randomised placebo-controlled trial of omalizumab has been performed in inducible urticarias but it has been reported to be effective in case reports.
IgE autoantibodies are also detected in a large number of patients with atopic dermatitis and bullous pemphigoid. In individual case reports, omalizumab treatment has been reported to be effective in some patients with these conditions. It has also been reported effective in chronic recurrent angioedema.
If you are not based in New Zealand, we suggest you refer to your national drug approval agency for further information about medicines (eg, the Australian Therapeutic Goods Administration and the US Food and Drug Administration) or a national or state-approved formulary (eg, the New Zealand Formulary and New Zealand Formulary for Children and the British National Formulary and British National Formulary for Children).
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