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Suppression of Lipid Mediators By the Humanized Anti-IgE Antibody Omalizumab in Aspirin-Exacerbated Respiratory Disease
Saturday, March 5, 2016: 2:00 PM
Room 502B (Convention Center)
Hiroaki Hayashi, MD, , , , , , , , , , , ,
Rationale: Research suggests that omalizumab is a potential treatment for severe allergic asthma. Aspirin-exacerbated respiratory disease (AERD) causes serious eosinophilic airway inflammation and mast cell activation. Compared with other types of severe asthma, omalizumab may have distinct therapeutic properties in AERD. This study investigated the efficacy of omalizumab for AERD, including changes in mast cell activation, urinary leukotriene E4 (LTE4) and prostaglandin D2 metabolite 9α,11β-prostaglandin F2 (PGD2M).

Methods: Japanese adults (n = 21) with AERD were enrolled at Sagamihara National Hospital between July 2009 and September 2013. All patients had received their usual asthma treatment for at least 12 months, and none of the patients had previously received omalizumab. The following parameters were measured at baseline and after 12 months of omalizumab treatment: urinary LTE4 and PGD2M concentrations; peripheral blood eosinophil count; respiratory function; and nasal and asthma-related symptom scores. The number of asthma exacerbations and hospitalizations, and daily systemic corticosteroid doses were also evaluated.

Results: Omalizumab significantly diminished median urinary concentrations (pg/mg of creatinine) of both LTE4 (703.2 [IQR: 234.9-2245.4] versus 167.7 [IQR: 72.3-296.5], reduction rate 76.2%; p=0.001) and PGD2M (55.5 [IQR: 14.8-96.5] versus 6.1 [IQR: 4.3-13.6], reduction rate 89.0%; p=0.002). Nasal and asthma-related symptom scores, the number of exacerbations and hospitalizations, and daily corticosteroid doses were also substantially reduced after omalizumab treatment.

Conclusions: Omalizumab was an effective treatment in AERD patients with severe asthmatic and nasal symptoms, and reduced mast cell activation and leukotriene overproduction.