4.1 Review

Biologics for eosinophilic granulomatosis with polyangiitis

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Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/ACI.0000000000000875

Keywords

biologics; benralizumab; eosinophilic granulomatosis with polyangiitis; mepolizumab; omalizumab; rituximab; severe asthma

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This review examines the potential use of anti T2 monoclonal antibodies as a treatment option for severe asthma and eosinophilic granulomatosis with polyangiitis (EGPA). It summarizes the pathophysiology of EGPA and provides an overview of the most reliable evidence from trials and real-life settings on the efficacy of anti T2 biologics in EGPA patients.
Purpose of reviewThe link between severe asthma and eosinophilic granulomatosis with polyangiitis (EGPA) in terms of pathophysiological background, clinical manifestations and disease evolution has leaded to investigate the relevance of anti T2 monoclonal antibodies licensed for severe asthma patients as a treatment option for EGPA. The present review aimed to provide un update on EGPA pathophysiology and to critically summarize the most robust evidence coming from trials and real-life setting on the use of anti T2 biologics in EGPA patients.Recent findingsMepolizumab, an anti-interleukin-5 monoclonal antibody, is the only biologic drug targeting eosinophilic inflammation currently approved for EGPA treatment at the dose of 300 mg/4 weeks. Its use is restricted by the American College of Rheumatology guidelines to specific diseases phases and severity grades. However the most appropriate mepolizumab positioning and dose is still under investigation in the real life practice, which is providing an increasing amount of evidence confirming its efficacy, alone or in combination with other options in different disease stages. The relevance of other monoclonal antibodies interfering with T2 inflammation, including omalizumab and benralizumab, is under investigation but the evidence is still scarceTaking into account the suboptimal medium-long term safety profile of conventional EGPA treatments, the opportunity of selectively targeting eosinophilic inflammation certainly represents a revolutionary approach. However, further real-word evidence is required to effectively position the new treatments in the light of the disease complexity, including different immunological drivers, and individual variability.

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