Treatment of chronic urticaria is challenging because many patients are refractory to or experience adverse effects with conventional therapy. Recently, short-term efficacy of omalizumab has been ...demonstrated.
To determine both the short- and long-term efficacy of omalizumab in the treatment of chronic urticaria.
Sixteen patients with severe chronic spontaneous urticaria at our center received omalizumab, 150 mg every 2 to 4 weeks, between 2010 and 2011. Disease severity was measured by urticaria activity scores before the first injection, during treatment, and at most recent follow-up, ranging from 9 to 24 months. Duration of therapy was determined individually for each patient. In this retrospective analysis, outcome measures include number of treatments required to induce remission and long-term remission sustainability.
Ten patients had remission of urticaria after their first injection (62%). Four patients required 2 to 6 treatments to achieve remission. Two patients discontinued treatment after 2 injections. Of the 14 patients who initially benefited (88%), 4 remain in remission more than 9 months after their last treatments. Seven patients continue to achieve remission with maintenance omalizumab, dosed at intervals appropriate for individual remission duration. Three patients became refractory and discontinued treatment (19%).
Omalizumab is an effective treatment for inducing and maintaining long-term remission for patients with severe chronic urticaria. Onset of remission is rapid, although duration is variable, with some patients requiring maintenance treatment. Large-scale randomized trials are necessary to confirm our findings that support the long-term efficacy of anti-IgE therapy for the treatment of this disease.
To the Editor: Chronic spontaneous urticaria (CSU) presents as recurrent itchy wheals, angioedema, or both for at least 6 weeks without a specific trigger.1 Roughly half of the patients with CSU ...achieve symptomatic control with H1-antihistamine therapy at approved doses, increased doses, or with additional therapies such as leukotriene receptor antagonists.1 CSU can be unpredictable and debilitating for patients because of a lack of clinical response.2 Recently, omalizumab, a neutralizing anti-IgE mAb, has gained approval for treatment of patients with CSU on the basis of evidence of substantial efficacy.3 However, the treatment benefit with omalizumab is usually lost when treatment is stopped. Specific IgE may target an endogenous antigen, a hypothesis supported by evidence that approximately 50% of patients with CSU have elevated levels of antithyroperoxidase IgE.5 Quilizumab, a humanized, afucosylated, monoclonal IgG1 antibody, binds membrane IgE at the M1-prime segment, which is absent in soluble IgE.6 In animal studies, quilizumab bound membrane IgE on IgE-switched B cells and plasmablasts and depleted them through apoptosis and antibody-dependent cell-mediated cytotoxicity.6 In clinical trials, quilizumab reduced serum total and specific IgE levels in healthy volunteers and in patients with allergic rhinitis or mild asthma.7,8 These reductions were sustained for at least 6 months after the last dose, suggesting that quilizumab affected long-term IgE memory.
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