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Multiple inflammatory mechanisms in eosinophilic oesophagitis make it unlikely that single pathway inhibition by monoclonal biological therapies would succeed
  1. Stephen E Attwood
  1. Health Services Research, Durham University, Morpeth, UK
  1. Correspondence to Professor Stephen E Attwood, Health Services Research, Durham University, Durham, UK; seaattwood{at}

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Once regarded as a rare disease, the incidence and prevalence of eosinophilic oesophagitis (EoE) have risen consistently over the past 25 years.1 It is now the second most common disease of the oesophagus after gastro-oesophageal reflux disease, and the most likely cause of thoracic dysphagia and of food bolus obstruction presenting to emergency departments.2 With the burden ever growing, it behoves clinicians who may see patients with symptoms suggestive of EoE to be aware of the condition, how it should be diagnosed and what the options are for treatment.

Confirmation of diagnosis is straightforward. A dense infiltration of eosinophils within the oesophageal epithelium with a peak count of ≥15 eosinophils/0.3 mm2 in any biopsy specimen is the distinguishing feature of EoE.2 While other conditions may also cause a degree of oesophageal eosinophilia, the threshold figure is a useful cut-off for diagnostic certainty.

Recent guidelines on EoE from the British Society of Gastroenterology/British Society of Paediatric Gastroenterology, Hepatology and Nutrition effectively standardise the diagnosis and assessment of the condition.2 However, they are less definitive about treatment since outcomes with traditional EoE therapies are relatively poor.

Proton pump inhibitors are a case in point. They result in at least partial symptom improvement in ~70% of patients with EoE, but histological remission in fewer than 50%.3 With an absence of clear usage instructions, off-label topical …

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  • Contributors SEA is the sole author of this editorial.

  • 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 The author has received payments for work as an advisory consultant or speaker for AstraZeneca, BristolMyersSquib, Dr Falk Pharma, GlaxoSmithKline and Regeneron Sanofi.

  • Provenance and peer review Commissioned; internally peer reviewed.

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