Corrado Pelaia1, Maria Teresa Busceti1, Claudia Crimi2, Giovanna Elisiana Carpagnano3, Nicola Lombardo4, Rosa Terracciano5, Alessandro Vatrella6, Girolamo Pelaia7. 1. Respiratory Medicine Unit, University "Magna Græcia" of Catanzaro - Catanzaro, Italy. 2. Department of Clinical and Experimental Medicine, University of Catania - Catania, Italy. 3. Department of Basic Medical Sciences, Neuroscience and Sense Organs, University of Bari - Bari, Italy. 4. Department of Medical and Surgical Sciences, University "Magna Græcia" of Catanzaro - Catanzaro, Italy. 5. Department of Experimental and Clinical Medicine, University "Magna Græcia" of Catanzaro - Catanzaro, Italy. 6. Department of Medicine, Surgery, and Dentistry, University of Salerno - Salerno, Italy. 7. Department of Health Sciences, University "Magna Græcia" of Catanzaro - Catanzaro, Italy. Electronic address: pelaia@unicz.it.
Abstract
BACKGROUND: The humanized monoclonal antibody benralizumab targets the α subunit of the interleukin-5 (IL-5) receptor and the FcγRIIIa receptor expressed by natural killer cells. Through this dual mechanism of action, benralizumab neutralizes the pro-eosinophil functions of IL-5 and promotes eosinophil apoptosis. OBJECTIVES AND METHODS: The present real-life study aimed to evaluate, in 22 allergic patients with severe eosinophilic asthma, the effects of benralizumab on asthma exacerbations and lung hyperinflation. RESULTS: In this regard here we show that, after 24 weeks of add-on treatment, benralizumab completely depleted peripheral blood eosinophils (from 810 to 0 cells/μL; p < 0.0001), and significantly decreased both asthma exacerbation number (from 4 to 0; p < 0.0001) and residual volume (from 2720 to 2300 mL; p < 0.01). Moreover, at the same time point (24 weeks) benralizumab also increased pre-bronchodilator FEV1 (from 1295 to 1985 mL; p < 0.0001), FVC (from 2390 to 2974 mL; p < 0.0001), FEF25-75 (from 0.6 to 1.42 L/sec; p < 0.0001), IC (from 1940 to 2460 mL; not significant), and ACT score (from 14.73 to 22.95; p < 0.0001), as well as reduced prednisone intake (from 25 to 0 mg; p < 0.0001). CONCLUSION: In conclusion, our results suggest that via its anti-eosinophil actions benralizumab improved airflow limitation, lung hyperinflation, and respiratory symptoms, as well as lowered asthma exacerbation rate and abrogated OCS consumption in most patients.
BACKGROUND: The humanized monoclonal antibody benralizumab targets the α subunit of the interleukin-5 (IL-5) receptor and the FcγRIIIa receptor expressed by natural killer cells. Through this dual mechanism of action, benralizumab neutralizes the pro-eosinophil functions of IL-5 and promotes eosinophil apoptosis. OBJECTIVES AND METHODS: The present real-life study aimed to evaluate, in 22 allergicpatients with severe eosinophilic asthma, the effects of benralizumab on asthma exacerbations and lung hyperinflation. RESULTS: In this regard here we show that, after 24 weeks of add-on treatment, benralizumab completely depleted peripheral blood eosinophils (from 810 to 0 cells/μL; p < 0.0001), and significantly decreased both asthma exacerbation number (from 4 to 0; p < 0.0001) and residual volume (from 2720 to 2300 mL; p < 0.01). Moreover, at the same time point (24 weeks) benralizumab also increased pre-bronchodilator FEV1 (from 1295 to 1985 mL; p < 0.0001), FVC (from 2390 to 2974 mL; p < 0.0001), FEF25-75 (from 0.6 to 1.42 L/sec; p < 0.0001), IC (from 1940 to 2460 mL; not significant), and ACT score (from 14.73 to 22.95; p < 0.0001), as well as reduced prednisone intake (from 25 to 0 mg; p < 0.0001). CONCLUSION: In conclusion, our results suggest that via its anti-eosinophil actions benralizumab improved airflow limitation, lung hyperinflation, and respiratory symptoms, as well as lowered asthma exacerbation rate and abrogated OCS consumption in most patients.
Authors: Carlos Martínez-Rivera; Ignasi Garcia-Olivé; Blanca Urrutia-Royo; Maria Basagaña-Torrento; Antoni Rosell; Jorge Abad Journal: BMC Pulm Med Date: 2021-01-21 Impact factor: 3.317
Authors: Francesco Menzella; Elena Bargagli; Maria Aliani; Pietro Bracciale; Luisa Brussino; Maria Filomena Caiaffa; Cristiano Caruso; Stefano Centanni; Maria D'Amato; Stefano Del Giacco; Fausto De Michele; Fabiano Di Marco; Elide Anna Pastorello; Girolamo Pelaia; Paola Rogliani; Micaela Romagnoli; Pietro Schino; Gianenrico Senna; Alessandra Vultaggio; Lucia Simoni; Alessandra Ori; Silvia Boarino; Gianfranco Vitiello; Elena Altieri; Giorgio Walter Canonica Journal: Respir Res Date: 2022-02-19