Eosinophilic oesophagitis is a chronic immune-mediated disease of the oesophagus. It is characterised by progressive oesophageal dysfunction due to tissue inflammation and fibrosis. The condition is more common in males and is typically seen in patients with a history of atopy.  Eosinophilic oesophagitis is estimated to affect around one in 1,000 people, although the prevalence appears to be rising in Australia.

The clinical features of this condition may include dysphagia, food impaction, and reflux-like symptoms. However, in children and infants, the presentation may involve food refusal, vomiting, weight loss, abdominal pain, or chest pain. The symptoms of eosinophilic oesophagitis can be difficult to distinguish from gastroesophageal reflux disease (GORD). While endoscopy may reveal characteristic changes, oesophageal biopsies showing an increased number of eosinophils throughout the oesophagus is required for diagnosis.

Eosinophilic oesophagitis is thought to be related to allergens in the diet or the environment. Dietary triggers may include dairy foods, egg, soy, wheat, nuts, and seafood. It can be difficult to identify specific trigger foods as the reactions are often delayed. Environmental triggers may include pollens, animals, dust mites, and moulds. Symptoms related to environmental triggers may occur seasonally, with treatment only required at certain times of the year. If this condition is not treated properly, oesophageal narrowing and strictures can occur as a result of chronic inflammation.

The first-line pharmacological treatment for eosinophilic oesophagitis is a proton pump inhibitor. Standard doses are used for four to eight weeks and, if a response is observed, therapy can continue using a maintenance regime as appropriate for GORD. A swallowed topical-acting corticosteroid can be added if symptoms persist.

The options for topical-acting corticosteroids are quite limited. Fluticasone metered-dose inhalers may be used for this purpose. Comprehensive patient counselling is required as the administration instructions differ significantly from those detailed in the consumer medicine information leaflet. In order to deliver the medication to the oesophagus, the patient should be advised to spray the dose into their mouth without inhaling and then swallow. Patients should also avoid eating and drinking in the 30 minutes after administration and, contrary to the usual instructions for corticosteroid inhalers, the patient should not rinse their mouth afterwards. It should also be noted that the dry powder formulation of fluticasone (i.e. the Accuhaler®) is not appropriate for this indication as these devices are breath-activated, so they cannot be used without inhaling.

Another topical corticosteroid recommended by the Therapeutic Guidelines is a budesonide slurry. A viscous mixture is achieved by combining the contents of one budesonide inhalation ampoule (1mg/2mL) with three to five grams of sucralose powder (e.g. the sugar substitute, Splenda®). The resulting mixture may then be swallowed after meals, usually twice daily.

Both of these topical-acting corticosteroids are used to treat eosinophilic oesophagitis on an ‘off-label’ basis. This may present some challenges as the administration instructions for eosinophilic oesophagitis are very different from the usual advice provided to manage respiratory conditions. The newly registered product, Jorveza®, overcomes these issues.

Jorveza® is the first product to be registered for the treatment of eosinophilic oesophagitis. It is presented as an orally disintegrating tablet containing 1mg of budesonide. Budesonide is delivered directly to the site of inflammation when the tablet is allowed to slowly dissolve on the tongue, with the patient gradually swallowing the dissolved material. Jorveza® tablets should not be taken with food or liquid, and patients should wait at least 30 minutes after a dose before eating, drinking, or performing oral hygiene.

The effectiveness and tolerability of budesonide orally disintegrating tablets were studied in a double-blind clinical trial. Adult patients with active eosinophilic oesophagitis were randomly assigned to receive budesonide 1mg twice daily or placebo for six weeks. The primary endpoint was the proportion of patients achieving both clinical and histologic remission at the end of treatment. This was reached in 57.6% of the budesonide group and 0% of the placebo group. Following a further six weeks of open-label induction, the rate of clinical and histologic remission was 84.7%. This suggests that prolonged treatment may be valuable to increase rates of remission.

The rate of just histologic remission was 93.2% in the budesonide group at six weeks (compared to 0% in the placebo group). This is much higher than the rates observed in previous trials for other budesonide formulations using higher doses. For example, a recent trial for a budesonide oral suspension showed only a 39% histologic response rate when dosed at 2mg twice daily. The study authors speculate that the formulations may be responsible for this difference. The effervescent qualities of the orally disintegrating tablets stimulate saliva production for around two or three minutes. During this time, small volumes of budesonide-containing saliva are continuously swallowed, which may result in superior oesophageal contact time.

Overall, budesonide orally disintegrating tablets were well-tolerated in this study. No patients in the budesonide group experienced serious adverse events or withdrew from the study due to treatment-emergent adverse effects. Suspected local fungal infection was more common in the budesonide group compared to the placebo group (23.7% versus 0%). However, symptomatic histologically-confirmed fungal infection occurred in only 5.1% of patients in the budesonide group. Like other systemically active glucocorticoids, budesonide may be associated with impairment of the hypothalamic-pituitary-adrenal (HPA) axis and reduced production of endogenous cortisol. In this trial, decreased plasma cortisol levels were detected in 5.1% of the budesonide arm (0% of the placebo group). Premature discontinuation of the therapy was not required, and levels normalised after the end of the study in each case.

Eosinophilic oesophagitis is a relatively newly identified condition, and understanding of its pathogenesis is currently limited. However, it is important that the condition is identified and treated appropriately to prevent permanent oesophageal damage.


  1. Dellon ES, Katzka DA, Collins MH, Hamdani M, Gupta S, Hirano I. Budesonide oral suspension improves symptomatic, endoscopic, and histologic parameters compared with placebo in patients with eosinophilic esophagitis. Gastroenterology 2016; 152(4): P776-86.e5.
  2. Gastrointestinal Expert Group. Therapeutic Guidelines: Gastrointestinal. Version 6. Melbourne: Therapeutic Guidelines; 2019.
  3. Jorveza® (Budesonide) Australian approved product information. Chatswood: De Falk Pharma. Approved September 2020.
  4. Lucendo AJ, Miehlke S, Schlag C, Vieth M, von Arnim U, Molina-Infante J, et al. Efficacy of budesonide orodispersible tablets as induction therapy for eosinophilic esophagitis in a randomized placebo-controlled trial. Gastroenterology 2019; 157(1): 74-86.e15.
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