Eosinophilic Gastrointestinal Diseases in 2026: Gastroenterology | March 26

Introduction

Eosinophilic gastrointestinal diseases (EGIDs) are chronic, immune-mediated disorders defined by eosinophil-predominant inflammation in the GI tract. Over the past 30 years, EGIDs—especially eosinophilic esophagitis (EoE)—have risen sharply without a clear plateau. This review summarises what has changed most in epidemiology, natural history, diagnosis, and treatment, and where the biggest gaps remain.

20 Key Takeaways (Clinician-focused)

Two big buckets: EGIDs are now classified as EoE (oesophagus only) and non-EoE EGIDs (stomach, small bowel, colon ± overlap).

New nomenclature matters: “Eosinophilic gastroenteritis” is being de-emphasised in favour of site-specific labels (EoG, EoN, EoC), improving clarity for care and research.

EoE is no longer rare: Incidence and prevalence have continued to climb globally, often faster than endoscopy/biopsy rates.

“Tip of the iceberg” problem: Many patients likely remain undiagnosed due to under-biopsying, missed follow-up after food bolus impaction, and diagnostic delay (often years).

High-yield clinical settings for EoE: EoE is common in dysphagia, extremely common in food impaction, and should be excluded before antireflux surgery or when strictures are present.

Atopy linkage is strong: Food allergy, asthma, eczema, and allergic rhinitis markedly increase EoE probability; risk rises with more atopic comorbidities.

Diagnosis of EoE is straightforward: Symptoms of oesophageal dysfunction + ≥15 eos/hpf on oesophageal biopsy + exclusion of competing causes.

Severity tracking is evolving: Tools like I-SEE help frame symptoms/complications, inflammatory activity, and fibrostenotic features over time.

Non-EoE EGIDs remain uncommon—but likely underrecognized: Prevalence is low in many datasets, but symptom nonspecificity and biopsy/reading variability may miss cases.

Non-EoE diagnosis is harder because eosinophils are “normal” distally: Unlike the oesophagus, eosinophils are normal residents in stomach/small bowel/colon—so thresholds and context matter.

Proposed histologic thresholds vary by segment: Practical cutoffs (approximate) increase from stomach/duodenum toward ileum/right colon and then decline leftward.

Non-EoE EGIDs can be mucosal, muscular, or serosal: Symptoms and complications reflect depth—muscular disease can obstruct; serosal disease can present with eosinophilic ascites.

Natural history of EoE is chronic and often progressive: Untreated inflammation can move toward fibrosis/stricture (fibrostenosis); risk increases with time and gaps in care.

EoE relapse is the rule when therapy stops: Multiple RCTs show high recurrence rates after withdrawing effective treatment.

EoE treatment pillars are now established: PPI, swallowed topical corticosteroids (STCs), food elimination diets (FEDs), and dupilumab are central options.

PPI is a legitimate anti-inflammatory strategy in EoE: About half achieve histologic remission; twice-daily dosing tends to perform better than once daily; maintenance can work for many responders.

STCs are highly effective and now disease-specific: Budesonide formulations (e.g., oral suspension/orodispersible tablet) have strong induction and maintenance data; candidiasis is the most common AE.

Dupilumab is the first approved biologic for EoE: It targets IL-4/IL-13 signaling and achieves meaningful histologic and symptom benefits, with a generally favourable safety profile.

Diet therapy is effective but should start simply: Empiric elimination is recommended, often beginning with the least restrictive (commonly milk elimination) and escalating stepwise if needed; allergy tests do not reliably identify triggers.

Non-EoE EGIDs: steroids still dominate; biologics are emerging: Evidence is mostly observational; systemic/topical steroids and elemental/elimination diets are used, while newer agents (e.g., IL-13 pathway drugs, dupilumab in EoG/EoN trials) are promising, but the field still lacks approved therapies and robust endpoints.