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Eosinophilic oesophagitis (EoE) is characterised by an abundance of oesophageal epithelial eosinophils.1 There is strong rationale that supports the eosinophil as central to the pathophysiology of EoE. In histology, the eosinophil is numerically the dominant inflammatory cell. Moreover, the eosinophil is capable of producing inflammation and tissue remodelling in human tissue. On degranulation, multiple destructive mediators are released that can invoke a robust inflammatory response. These include eosinophil proinflammatory cationic proteins (MBP, EDN, EPO, ECP), chemokines and cytokines (IL-4, IL-5, IL-13, TGF-β, etc) that regulate cell chemoattraction and activation, perpetuate inflammation, and instigate epithelial mesenchymal transition associated with subepithelial fibrosis.2 Indeed, first-line therapies in EoE include swallowed topical corticosteroids and elimination diets that concomitantly improve oesophageal eosinophilia as well as endoscopic disease activity and EoE-related symptoms.3 4 Further supporting an important role for the eosinophil in EoE is its importance in other type 2 inflammatory or atopic diseases including asthma and allergic rhinitis. These lines of evidence supported the use of the peak eosinophil count (PEC) as a primary endpoint for therapeutics in EoE.
In Gut, a well-executed, systematic review and network meta-analysis was performed to evaluate the efficacy of pharmacological approaches for EoE based on 15 randomised, controlled clinical trials.5 The relative efficacy of therapeutics was based on comparisons of the PEC following treatment for variable durations of induction therapy ranging from 6 to 24 weeks. For achieving histological remission (defined as a PEC≤6 eosinophils/high power field), lirentelimab (a monoclonal antibody for the Siglec 8 receptor), budesonide orodispersible tablet (a formulation approved by the European Medicines Agency but not the US Food …
Contributors Both DK and IH contributed to the writing of this commentary.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests DK has received research funding from Shire, a Takeda company; and a consulting fee from Receptos/Celgene/Bristol Myers Squibb. IH has received research funding from Adare Pharmaceuticals/Ellodi Pharmaceuticals, Allakos, Arena Pharmaceuticals, AstraZeneca, Meritage Pharma, Receptos/Celgene/Bristol Myers Squibb, Regeneron Pharmaceuticals and Shire, a Takeda company; and is a consultant for Adare Pharmaceuticals/Ellodi Pharmaceuticals, Allakos, Amgen, Arena Pharmaceuticals, AstraZeneca, Dermavant, EsoCap Biotech, GlaxoSmithKline, Gossamer Bio, Lilly, Parexel/Calyx Clinical Research Solutions, Nexstone, Phathom Pharmaceuticals, Receptos/Celgene/Bristol Myers Squibb, Regeneron Pharmaceuticals, Sanofi and Shire, a Takeda company.
Provenance and peer review Commissioned; internally peer reviewed.