Letter to the Editor
Long-term treatment of refractory severe chronic urticaria by omalizumab: analysis of two cases

Omalizumab is a recombinant humanized monoclonal antibody raised against the Cε3 domain of human IgE, whose efficacy and safety in the treatment of moderate to severe asthma has been demonstrated [1–3]. Several other possible indications for this innovative drug have been considered, including severe idiopathic urticaria [4–6].
Here we report on two stubbornly refractory cases successfully treated with omalizumab.
Case 1. A Caucasian housewife and part-time domestic caretaker, aged 50. Since 2002, she had been suffering from severe idiopathic urticaria. Giant, intensively itchy lesions were often (but not always) elicited by pressure.
Previous unsuccessful therapies comprised: high-dose antihistamine (including ketotifen); leukotriene modifiers; dapsone; cyclosporine (4 mg/kg/day); bromazepam; and prolonged low to mid-dose corticosteroid courses.
At presentation, the patient had been treated with betamethasone (1 mg/day) for 2 years, consecutively, in association with various antihistamines at high dosage (up to 4 times the standard dosage). Moreover, she was following a rather restricted “hypo-allergic” diet. In spite of this therapeutic regimen, she was fully symptomatic, with daily eruptions of large itchy wheals, appreciable scratching lesions, and severe pruritus. The current 7-day Urticaria Activity Score (UAS) [7] was > 38. Total IgE count was 170 kU/l. Other allergy and immunology tests were negative, including auto-immunity tests. However, the autologous serum test was positive (undiluted), compatible with the presence of possible autoimmune pathogenic mechanisms (e.g. autoantibodies to IgE or to the α chain of the high affinity IgE receptor FcεRI).
After discontinuation of the corticosteroid therapy and an additional attempt at controlling the symptoms with fexofenadine and cyproheptadine (which failed), we started the treatment with omalizumab (off-label; 300 mg/month; the dose was calculated according to the standard schedule for severe asthma; body weight was 52 kg).
The monoclonal antibody produced a dramatic and almost immediate (2 days) clinical improvement. Antihistamine therapy (fexofenadine 180 mg daily and ketotifen 2 mg b.i.d.) was initially needed in order to achieve full symptom control (7-day UAS Ξ 0). After 9 months we decided to raise the omalizumab dosage to 450 mg/month. That enabled discontinuation of the antihistamine therapy. As at March 2014, the patient has been under omalizumab...


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