Background: Type 2 (T2) inflammation, characterized by blood and airway eosinophilia, underlies severe eosinophilic asthma (SEA) and chronic rhinosinusitis with nasal polyps (CRSwNP). In line with the Global Airways theory, SEA and CRSwNP frequently co-occur, creating a multimorbid phenotype. Separately, SEA and CRSwNP are burdensome: when concomitant, they compound each other, creating a more difficult-to-treat disease with increased complications. Body: Current management approaches rarely control disease and are associated with substantial side-effects. Several recently developed anti-IL-5 monoclonal antibodies have shown efficacy in treating co-morbid SEA with CRSwNP by targeting T2 inflammation with systemic therapies. Of these, only benralizumab directly targets the IL-5 receptor-α, leading to rapid, sustained, near-complete eosinophil depletion. Analyses in patients with co-morbid SEA with CRSwNP are limited, although data from the ANDHI, XALOC-1, and RANS studies suggest benralizumab can effectively target inflammation underlying co-morbid disease. Conclusion: Despite progress toward more effective therapies, treatment approaches remain siloed, with SEA and CRSwNP often managed separately. There is a need for the development of multidisciplinary approaches for treating patients with comorbid SEA with CRSwNP.
Benralizumab and the integrated management of co-morbid severe eosinophilic asthma with chronic rhinosinusitis with nasal polyps
de Corso E.;
2025
Abstract
Background: Type 2 (T2) inflammation, characterized by blood and airway eosinophilia, underlies severe eosinophilic asthma (SEA) and chronic rhinosinusitis with nasal polyps (CRSwNP). In line with the Global Airways theory, SEA and CRSwNP frequently co-occur, creating a multimorbid phenotype. Separately, SEA and CRSwNP are burdensome: when concomitant, they compound each other, creating a more difficult-to-treat disease with increased complications. Body: Current management approaches rarely control disease and are associated with substantial side-effects. Several recently developed anti-IL-5 monoclonal antibodies have shown efficacy in treating co-morbid SEA with CRSwNP by targeting T2 inflammation with systemic therapies. Of these, only benralizumab directly targets the IL-5 receptor-α, leading to rapid, sustained, near-complete eosinophil depletion. Analyses in patients with co-morbid SEA with CRSwNP are limited, although data from the ANDHI, XALOC-1, and RANS studies suggest benralizumab can effectively target inflammation underlying co-morbid disease. Conclusion: Despite progress toward more effective therapies, treatment approaches remain siloed, with SEA and CRSwNP often managed separately. There is a need for the development of multidisciplinary approaches for treating patients with comorbid SEA with CRSwNP.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
