The following is a summary of “Eosinophil depletion with benralizumab is associated with attenuated mannitol airway hyperresponsiveness in severe uncontrolled eosinophilic asthma,” published in the MARCH 2023 issue of Allergy & Immunology by Chan, et al.

People with persistent asthma often have airway hyperresponsiveness (AHR) and eosinophilia. For a study, researchers sought to determine if using benralizumab to deplete eosinophils could reduce indirect mannitol AHR in patients with severe uncontrolled asthma.

The study was conducted using an open-label design. Participants were adults with uncontrolled severe eosinophilic asthma who had received usual inhaled corticosteroids and/or long-acting β-agonist for four weeks prior to the study. They were given three doses of benralizumab 30 mg every four weeks, followed by 16 weeks of washout after the last dose. The primary outcome was the doubling difference (DD) in the provocative dose of mannitol required to decrease FEV₁ by 10% (PD₁₀) at the endpoint after 12 weeks. Secondary outcomes included measures assessed by the asthma control questionnaire and mini-asthma quality of life questionnaire.

A total of 21 patients completed 12 weeks of benralizumab therapy. Their mean age was 53 years (SEM = 4), FEV₁ was 80.2% (SEM = 4.1%), and their inhaled corticosteroid dose was 1,895 μg (SEM = 59). Of the 21 patients, 12 received long-acting muscarinic antagonist, and 13 received leukotriene receptor antagonists. A significant improvement in AHR was observed at week 8, with a mean change in PD₁₀ of 2.1 DD (95% CI 1.0, 3.3; P < .01) at week 12. Mean changes in the asthma control questionnaire and mini-asthma quality of life questionnaire were significant at week 2 and sustained over 12 weeks, exceeding the minimal important difference. Peripheral blood eosinophils were depleted by 2 weeks (439 to 6 cells/μL). However, no significant improvement in lung function was observed after 12 weeks. Domiciliary peak flow and symptoms improved with benralizumab.

Eosinophil depletion causes a clinically significant attenuation of the AHR in patients with severe, uncontrolled asthma.

Reference: jacionline.org/article/S0091-6749(22)01510-X/fulltext