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Eosinophilic oesophagitis (EOE)

“Eosinophilic esophagitis represents a chronic immune/antigen mediated oesophageal disease characterized clinically by symptoms related to oesophageal dysfunction and histologically by eosinophil-predominant inflammation” (80), as defined by a multidisciplinary panel in 2011.

The American College of Gastroenterology define EOE as: ‘The presence of symptoms related to oesophageal dysfunction such as dysphagia, food impaction, chest pain, etc.’

  • Oesophageal mucosa with eosinophil-predominant inflammation, up to 15 eosinophils per high power field.
  • Mucosal eosinophils limited to the oesophagus and persist after a trial of PPIs.
  • Exclusion of secondary causes of oesophageal eosinophilia. (39)

There is a higher prevalence of EOE in adolescents and adults born with OA/TOF. The prevalence in the general population is <4/10000, compared with 9.5% prospectively biopsied adolescents born with OA/TOF. (75,48)

The causes of this are thought to be multifactorial. One cause is the high prevalence of GORD in the TOF population, exposing the oesophagus to injury and damaging the mucosa. This damage to the mucosal barrier allows easier penetration of allergens. Secondly, the near universal dysmotility of the oesophagus increases contact time between food/allergens and the oesophageal mucosa, leading to chronic irritation which triggers increased mucosal permeability to allergens and the influx of eosinophils and mast cells.

It is difficult to differentiate EOE and severe GORD from symptoms alone. In one study, patients with EOE had higher levels of dysphagia, retrosternal pain and food impaction, but some in patient groups with repaired OA/TOF and those without EOE reported these symptoms. (81)


  • Referral for oesophagogastroduodenoscopy (OGD) and oesophageal biopsy
  • Full blood count may show peripheral eosinophilia


This is known as the 3Ds: diet, drugs and dilatation. Either drugs or diet can be used as first-line treatment. In OA/TOF patients there may be a greater proportion of patients that respond to PPI treatment as a first-line therapy. (212)

  1. Oral steroids are the mainstay here, either budesonide oral dispersible tablet, which dissolves in the mouth over two minutes, swallowed by saliva, or swallowing post use of multi-dose inhalers (eg fluticasone, mometasone, beclomethasone) so that the steroid reaches the oesophagus rather than the traditional aim of the airways. Patients should then avoid eating and drinking for 30 to 60 mins post steroid to keep the steroid in place. This is initiated for eight weeks, then success judged by repeat OGD and biopsy.
  2. This is an elimination diet, again followed strictly for six to eight weeks, then reinvestigated by OGD and biopsy. An elimination diet should only be undertaken with input from a dietitian as part of a tertiary centre multidisciplinary team (MDT) looking after EOE patients. The diet may be a six-food elimination diet (dairy, wheat, egg, soya, nuts and seafood) or an elemental diet.
  3. This is needed in those patients with signs of strictures and stenosis, but does not treat the underlying EOE leading to the formation of strictures. (82)

The European Society for Paediatric Gastroenterology, Hepatology and Nutrition guidelines state that EOE needs to be excluded in OA patients of all ages with dysphagia, reflux symptoms, coughing, choking or recurrent strictures that are refractory to PPI, before proceeding to anti-reflux surgery. (39)