Exploring the Link Between Atopic Dermatitis and Eosinophilic Esophagitis

Eosinophilic Oesophagitis (EoE), or Esophagitis in American spelling, is the most common of the eosinophilic gut disorders, occurring in approximately 1 in 700 people.

EoE and Atopic Dermatitis (AD) are both type 2 helper T-cell (Th2)–mediated diseases. They can occur together and share overlapping immune pathways.

A recent narrative review published in the Journal of Clinical and Aesthetic Dermatology highlights the clinical and immunological connections between these two conditions, pointing to new areas for research and therapy.

Within our community, around 80% of members report additional atopic conditions, such as immediate food allergies, asthma, allergic rhinitis (AR), and AD.

Shared Mechanisms

EoE shares clinical features, immunologic pathways, susceptibility loci, and risk with these conditions.

Both conditions involve an impaired immune response to antigens or allergens. This leads to CD4+ Th2 differentiation and excess production of immunoglobulin E (IgE).

The coexistence of EoE and AD is an emerging area of study. Both manifest on stratified squamous epithelium — in the oesophagus and skin — and both may respond to similar treatments, including avoidance of triggers, topical steroids, and dupilumab.

Disease Endotypes

Endotypes are subtypes of disease defined by molecular mechanisms underlying visible clinical features. They can be classified using histologic, endoscopic, and molecular data.

  • For EoE, three distinct endotypes have been identified, which has greatly improved understanding of its pathogenesis.
  • For AD, proposed classifications exist, but no consistent endotype model has yet been confirmed.

A table featuring Endotypes of Eosinophilic Oesophagitis

Table 1. Endotypes of Eosinophilic Oesophagitis, Source

Pathogenesis

The development of both EoE and AD involves a complex interplay of genetics, immune dysregulation, and environmental influences.

Key factors include:

  • Gut–skin axis: the gut microbiome plays a crucial role in maintaining mucosal immunological tolerance. Alterations in gut bacteria can increase vulnerability to immune-related skin conditions.
  • Environmental influences: stress, diet, pollutants, and climate change can affect the microbiome and damage epithelial barriers.
  • Barrier dysfunction: tight junction proteins help seal the spaces between cells, especially in the skin and gut, forming a protective barrier. Loss of these proteins, as well as defects in barrier proteins such as filaggrin, involucrin, and SPRPs, weakens protection and allows allergens to penetrate.
  • Immune response: both conditions are driven by a Th2-type immune response. In EoE, damage to the oesophageal barrier enables allergens to enter, triggering immune cells like eosinophils and mast cells. These cells release IL-5 and IL-13, leading to inflammation and tissue damage.

Figure 1: Th2-driven basis for atopic dermatitis and EoE, Source

The epithelial barrier hypothesis suggests that environmental and microbial disruptions of the skin and mucosal barriers contribute to the global rise of allergic and chronic diseases.

  • In AD, up to 90% of patients show colonisation with Staphylococcus aureus, which drives skin inflammation.
  • In EoE, limited data suggest that microbiome disruption (e.g., increased Haemophilus species in untreated cases) and early-life antibiotic use may be linked to EoE development, although more research is needed.

Treatment

  • Both AD and EoE are treated with topical steroids, avoidance of allergens, and dupilumab, a biologic targeting IL-4 and IL-13.
  • Elimination diets and allergen immunotherapy may be beneficial, but the evidence is limited, and responses vary.
  • AD patients with symptoms like trouble swallowing, food impactions, or acid reflux should be evaluated for EoE.
  • Multidisciplinary care and biologic therapy are recommended for patients with overlapping atopic conditions.

Conclusion

EoE and AD are distinct but co-existing diseases with shared immune pathways, overlapping symptoms, and increasing prevalence. Both are driven by Th2 inflammation, particularly involving IL-13.

Key takeaways:

  • Clinicians should be alert to EoE symptoms such as swallowing difficulties and food impactions in AD patients to avoid missed or delayed EoE diagnoses.
  • Elimination diets remain an option in EoE but are not recommended for those with co-comitant AD, where biologics are recommended as a more effective treatment.
  • Shared therapies include topical steroids and dupilumab, while emerging biologics (e.g., tralokinumab, JAK inhibitors) may expand options in the future.

References:

Jaros, J., Ahuja, K., & Lio, P. (2025). Exploring the link between atopic dermatitis and eosinophilic esophagitis: A narrative review. Journal of Clinical and Aesthetic Dermatology, 18(3), 15–20. https://jcadonline.com/link-between-atopic-dermatitis-eosinophilic-esophagitis/

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Author: Olena Filatova

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