Omalizumab-Induced Aspirin Tolerance in Nonsteroidal Anti-Inflammatory Drug-Exacerbated Respiratory Disease Patients Is Independent of Atopic Sensitization.

ABSTRACT

BACKGROUND: Nonsteroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (N-ERD) comprises the triad of chronic rhinosinusitis with nasal polyps (CRSwNP), asthma, and intolerance to inhibitors of the cyclooxygenase-1 enzyme. The impact of omalizumab on prevention of aspirin-induced hypersensitivity in N-ERD patients with and without atopic sensitization has not been thoroughly addressed. OBJECTIVE: To investigate the effect of omalizumab treatment on aspirin tolerance in atopic and nonatopic N-ERD patients. METHODS: This single-center, prospective trial evaluated overall omalizumab-induced aspirin tolerability in N-ERD patients by performing aspirin challenge testing before and after 6 months of anti-immunoglobulin E (IgE) therapy. The impact of omalizumab on CRSwNP asthma as well as serum and tissue biomarkers in patients with and without comorbid atopic sensitizations was further analyzed. RESULTS: Out of 33 patients included in the study, 56% developed complete aspirin tolerance and 18% tolerated higher dosages after 24 weeks. Polyp size and disease-specific symptoms (nasal polyp score [NPS] -1.9 ± 0.3, P < .001; Sino-Nasal Outcome Test [SNOT]-20 -16.7 ± 3.7, P < .001; Asthma Control Test [ACT] 3.2 ± 0.7, P < .001) improved in all patients irrespective of atopic sensitization. Effectiveness of omalizumab was accompanied by an increase in mean total serum IgE (307.8 ± 42 kU/L; P < .001) and a decrease in eosinophilic cationic protein (-10.6 ± 6.7 µg/L) and in relative eosinophilia (-2.5 ± 0.7%; P < .01). Whereas there was a significant reduction of tissue IgE (P < .05) in all patients after 4 weeks, the number of local eosinophils decreased only in atopic individuals (P < .05). CONCLUSIONS: Omalizumab induced complete aspirin tolerance in the majority of patients (56%) independent of atopic sensitization and demonstrated clinical efficacy in the treatment of CRSwNP and asthma. Inhibition of IgE can therefore be a promising treatment option in preventing NSAID hypersensitivity reactions in N-ERD patients.