A severe adverse reaction to omalizumab therapy in chronic spontaneous urticaria

Omalizumab is a humanized IgG1-k monoclonal antibody(mAb), which binds the C3 domain of free IgE, inhibiting its interaction with the high-affinity IgE receptor (FcεRI) on the surface of basophils, mast cells, and dendritic cells (Lieberman, Jones, Rajwanshi, Rosén, & Umetsu, 2017). Adverse events to omalizumab have been rarely described (Lieberman et al., 2017; Perino, Freymond, Devouassoux, Nicolas, & Berard, 2018). Specifically, anaphylaxis was reported in 0.1 to 0.2% of patients, but the underlying mechanism remains unknown (Lieberman et al., 2017). Adverse events of omalizumab may depend on the murine component of the drug or may be due to specific excipients (Lieberman et al., 2017). A 33-year-old Caucasian woman presented to our department in February 2019 with a 2-year history of antihistamine-resistant chronic spontaneous urticaria (CSU) with only partial response to oral corticosteroids. The patient underwent screening tests for CSU. Laboratory investigations for basophil activation test (BAT) and for an autoimmunity panel were negative. Total IgE count was 187 UI/mL, while Ddimer, fibrinogen, and eosinophils were in the normal range. According to the personal medical history, we decided to start subcutaneous omalizumab 300 mg. About 12 hr after the first administration, the patient experienced pyrexia (body temperature: 37.5 ) and headache with resolution after a few days. A general remission of urticaria was also observed. About 24 hr after the second administration, the patient developed a severe diffuse painful urticarial rash (UAS7: 42) (Figure 1) associated with systemic symptoms of vomiting, mucous diarrhea, and diffuse muscular pain, poorly responsive to both oral antihistamine (ebastine 10 mg twice/day) and steroids (methylprednisolone 16 mg twice daily for a week, then betamethasone 4 mg intramuscular twice daily for 2 days). Blood tests were performed, resulting within normal range, except for an