Dietary Management of Eosinophilic Esophagitis: Tailoring the Approach

Abstract

Eosinophilic esophagitis (EoE) is a unique form of non-immunoglobulin E-mediated food allergy, restricted to the esophagus, characterized by esophageal eosinophil-predominant inflammation and dysfunction. The diagnosis requires an esophago-gastroduodenoscopy with esophageal biopsies demonstrating active eosinophilic inflammation with 15 or more eosinophils/high-power field, following the exclusion of alternative causes of eosinophilia. Food allergens trigger the disease, withdairy/milk, wheat/gluten, egg, soy/legumes, and seafood the most common. Therapeutic strategies comprise dietary restrictions, proton pump inhibitors, topical corticosteroids, biologic agents, and esophageal dilation when strictures are present. However, avoidance of trigger foods remains the only option targeting the cause, and not the effect, of the disease. Because EoE relapses when treatment is withdrawn, dietary therapy offers a long-term, drug-free alternative to patients who wish to remain off drugs and still be in remission. There are currently multiple dietary management strategies to choose from, each having its specific efficacy, advantages, and disadvantages that both clinicians and patients should acknowledge. In addition, dietary regimens should be tailored around each individual patient to increase the chance of tolerability and long-term adherence. In general, liquid elemental diets devoid of antigens and elimination diets restricting causative foods are valuable options. Designing diets on the basis of food allergy skin tests results is not reliable and should be avoided. This review summarizes the most recent knowledge regarding the clinical use of dietary measures in EoE. We discussed endpoints, rationale, advantages and disadvantages, and tailoring of diets, as well as currently available dietary regimens for EoE.

Diet Therapy in Eosinophilic Esophagitis. Focus on a Personalized Approach

“…Although the elemental diet can induce a rapid disease-remission in only 2 weeks, several disadvantages limit its adherence ( Table 2 ) ( 43 ). The poor palatability, highly restrictive nature, costs, and psychosocial isolation are the main reasons for treatment discontinuation and low compliance ( 12 , 17 , 27 ).…”

“…Once clinical and histologic remission is achieved, a single food or food group is gradually reintroduced based on the specific diet approach. The endoscopy should be made after 4–6 weeks each reintroduction to confirm or exclude disease remission and before proceeding to other food reintroduction ( 2 , 28 , 43 ). Food reintroduction should start from the less allergenic foods (fruits and vegetables) to the most common food triggers ( 52 ).…”

“…Once the culprit food(s) is identified, the long-term diet therapy is only based on exclusively avoiding the food(s) responsible for esophageal inflammation ( 55 ). In adults, the strict avoidance of trigger food(s) maintains a complete remission (clinical and histologic remission) for up to 3 years ( 43 , 56 ). Notably, the prolonged elimination of a food or a group of trigger foods might induce potential nutritional deficiency.…”

Esophageal dysmotility in patients with eosinophilic esophagitis: pathogenesis, assessment tools, manometric characteristics, and clinical implications

“…Nevertheless, it is estimated that EoE is diagnosed with a mean delay of up to 10 years [ 3 , 4 ]. The disease is characterized by a chronic eosinophil-predominant inflammation restricted to the esophagus triggered by the exposure to food or inhalant antigens, which causes symptoms of esophageal dysfunction [ 5 ]. The diagnosis is made based on the presence of at least 15 eosinophils/HPF (high-power field) in at least one esophageal biopsy in combination with a suggestive clinical history, following the exclusion of secondary causes of eosinophilia [ 6 , 7 ].…”

“…In this regard, eosinophilic and mast cells products have been shown to affect visceral motility and function in EoE via several mechanisms [ 10 ]. Additionally, there is modest correlation among histology, endoscopy, and clinical disease activity in EoE [ 5 , 11 ] and esophageal dysmotility may be a contributing factor to this discrepancy.…”