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CC BY 4.0 · Journal of Digestive Endoscopy
DOI: 10.1055/s-0045-1813225
Editorial

Eosinophilic Esophagitis in India: Low Prevalence, Emerging Insights, and Therapeutic Frontiers

Autoren

  • Manjeet K. Goyal

    1   Department of Internal Medicine, Cleveland Clinic, Akron General, Cleveland, Ohio, United States

  • Praneet Wander

    2   Division of Gastroenterology, St Mary's Hospital, Trinity Health of New England, Waterbury, Connecticut, United States

  • Omesh Goyal 

    3   Department of Gastroenterology, Dayanand Medical College and Hospital, Ludhiana, Punjab, India

Funding None.
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Eosinophilic esophagitis (EoE) is a clinicopathological disorder characterized by dense eosinophil infiltration of the esophageal mucosa—at least 15 eosinophils per high-power field—and symptoms such as heartburn, chest pain, and dysphagia.[1] Because these symptoms overlap with those of functional esophageal disorders, the Rome IV criteria advocate ruling out EoE before labeling the patient as functional esophageal disorder.[2] EoE was long underrecognized as most of the patients with gastroesophageal reflux disease (GERD)-like symptoms are usually treated empirically with proton-pump inhibitors (PPIs) without further evaluation.[2] Once researchers appreciated that some patients with GERD-like symptoms and eosinophilic esophagitis did not respond to PPIs, it became evident that EoE is a distinct condition requiring targeted diagnosis and management.

The worldwide epidemiology of EoE has shifted dramatically in the past two decades. Population-based studies suggested a pooled prevalence of roughly 22.7 per 100,000 and an annual incidence around 3.7 per 100,000.[3] High-income countries have reported prevalence rising above 34 per 100,000 and incidence approaching 7.7 per 100,000 adults.[4] Asia, once considered largely free of EoE, is now experiencing growing detection. A Japanese registry reported an incidence of 2.82 per 100,000 and prevalence of 10.68 per 100,000, whereas a meta-analysis documented an increase from 19.8 to 73 per 100,000 in the region between 2005 to 2009 and 2015 to 2019.[5] These figures illustrate that EoE is not solely a Western disease and that improved awareness and surveillance can reveal cases that previously went undiagnosed. In India, however, published data remain scarce, prompting investigators to assess how frequently EoE occurs among patients with reflux-like symptoms.[6] [7]

In study by Mittal et al published in the current issue of the Journal of Digestive Endoscopy, 350 adults presenting with upper gastrointestinal complaints underwent upper endoscopy with systematic biopsies of the proximal and distal esophagus, stomach, and duodenum.[8] Histopathology was used to count eosinophils and exclude secondary causes. Symptom severity was measured with a visual analogue scale, and PPI responsiveness was defined as a 50% or greater reduction after 8 weeks of therapy. Endoscopic findings were classified as normal mucosa, reflux esophagitis, or features suggestive of EoE such as mucosal edema, white plaques, furrows, rings, and strictures. Among the 350 participants, only four met histologic criteria for EoE, yielding a prevalence of 1.14%. These cases were predominantly male, around 40 years of age, and had longer symptom duration than the rest of the cohort. Three of the four EoE patients reported a personal or family history of allergic disease. While heartburn occurred in most study participants, dysphagia, and food impaction were disproportionately observed in the EoE group; 75% of EoE patients reported dysphagia compared with 4.6% of the overall cohort. Notably, three of the four EoE cases failed to improve after an 8-week PPI trial. These findings underscore that clinicians should suspect EoE when dysphagia coexists with atopic history and PPI refractory symptoms. They also highlight the importance of obtaining biopsies from patients whose symptoms persist despite acid suppression.

The authors report that dysphagia, history of allergy, and food bolus impaction were the strongest predictors of EoE, whereas abdominal pain and heartburn were not discriminatory. Patients diagnosed with EoE also had higher peripheral eosinophil counts and were more likely to be PPI nonresponders. Despite the small number of cases, these clinical characteristics align with the global literature and emphasize that EoE should be considered when typical reflux symptoms coexist with dysphagia and atopy. The investigators concluded that EoE is uncommon in northern India but recommended maintaining a high index of suspicion in patients with dysphagia, atopic comorbidities, and poor response to PPIs.

The role of eosinophils in gastrointestinal disorders is being increasingly recognized.[9] Understanding why eosinophils accumulate in the esophagus requires appreciating the disease's complex pathogenesis. EoE is now recognized as an antigen-driven type 2 inflammatory disorder. Allergen-induced activation of esophageal epithelial cells triggers a dysregulated feed–forward cycle in which impaired epithelial barrier integrity allows allergens to penetrate deeper layers.[10] Dendritic cells, innate lymphoid cells, and T helper 2 lymphocytes then produce cytokines such as interleukin-5, interleukin-13 and thymic stromal lymphopoietin, recruiting eosinophils, mast cells, and basophils that further damage the barrier.[11] Genetics play a role: variants in genes encoding barrier proteins (e.g., filaggrin and desmoglein-1) or regulatory proteins (e.g., CAPN14 and TSLP) are associated with increased risk, and early life factors like antibiotics, cesarean delivery, and acid suppression may interact with this genetic backdrop. Over time, chronic inflammation causes basal zone hyperplasia, dilated intercellular spaces, and fibrosis, leading to esophageal rings and strictures.

Treating EoE requires targeting both inflammation and structural complications. PPIs were once used solely to distinguish EoE from GERD, but early observations showed that approximately 40% of patients with esophageal eosinophilia and half of adults achieved clinical and histologic remission on high-dose PPIs even without abnormal pH monitoring.[12] This phenomenon led to the concept of “PPI-responsive esophageal eosinophilia” and raised the question of whether EoE and acid-mediated esophagitis might overlap. Subsequent guidelines now view PPIs as a treatment rather than a diagnostic test; they recommend PPIs, dietary elimination or topical corticosteroids as equivalent first-line therapies. A 2025 cost-utility analysis reported that these three options have similar effectiveness and cost in pediatric patients, reinforcing the idea that therapy should be individualized.[13]

Other treatments are available when PPIs fail or patients prefer alternatives. Swallowed topical corticosteroids such as fluticasone or budesonide reduce eosinophilic inflammation and induce remission in roughly two-thirds of patients. Elimination diets, which remove suspected food antigens, range from simple exclusion of cow's milk to a six-food elimination (dairy, wheat, eggs, soy, nuts, and seafood). Meta-analyses report histologic remission rates of 50 to 61% for four- or six-food elimination diets and up to 72% for elemental formulas, though adherence can be challenging. For fibrostenotic disease, esophageal dilation relieves obstruction but does not address underlying inflammation. Biologics are an emerging frontier: dupilumab, an antibody targeting the IL-4 receptor α chain, blocks IL-4 and IL-13 signaling and has become the first biologic approved for EoE. It is particularly useful for patients who are PPI refractory or cannot tolerate steroids or strict diets, although cost and injection requirements limit widespread use.

The Indian study's finding that most EoE cases were PPI nonresponders echoes evidence that only half of patients achieve histologic remission with high-dose PPIs.[1] [8] The low prevalence reported (1.14%) may encourage complacency, yet the global trend toward increasing incidence and the growing recognition of EoE in Asia caution against such an approach.[5] Importantly, the presence of heartburn and reflux esophagitis in many non-EoE patients underscores that GERD remains common; nonetheless, the coexistence of dysphagia, atopic history, and PPI failure should prompt biopsy to exclude EoE.

The current study has several strengths: prospective design, systematic biopsies from multiple esophageal sites, and use of validated symptom scales. Still, limitations include the hospital-based sample, which may not reflect community prevalence, and the small number of EoE cases. Absence of pH monitoring could mean that some PPI nonresponders were misclassified, and follow-up was not long enough to assess outcomes after treatment. More multicenter studies across India are necessary to confirm whether EoE is truly rare or simply underrecognized.

Future studies should explore genetic and environmental factors that might explain why EoE appears less common in India. Investigating early life exposures, diet, microbiome composition, and helminth infections could provide insights into protective factors. Clinicians should adopt standardized biopsy protocols and include EoE in the differential diagnosis of chronic dysphagia to reduce diagnostic delays. Research into step-up elimination diets, real-world effectiveness of topical steroids, and cost-effectiveness of biologics will help optimize treatment. Endotypic profiling (inflammatory vs. fibrostenotic forms) may guide therapy choices, and combining therapies (e.g., PPIs plus elimination diets) could be explored to improve outcomes.

EoE has emerged from obscurity to become one of the leading causes of dysphagia and food impaction in young adults. The evidence that dysphagia, atopic history, elevated eosinophil counts, and PPI nonresponsiveness predict EoE should encourage clinicians to pursue early diagnosis. Because only about half of patients will achieve remission with PPIs and dietary adherence can be difficult, a patient-centered approach that offers alternatives such as topical steroids, elimination diets, and biologics is essential.[14] Continued research, guideline dissemination, and clinician education will enable better recognition and management of this complex disease.

Patient Consent

Informed consent in the local language was obtained from all study participants.




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Artikel online veröffentlicht:
18. November 2025

© 2025. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/)

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