Letter: Helicobacter pylori and Eosinophilic Oesophagitis—Lost in Definition?

We read with interest the meta-analysis by Spinelli et al. which reported a 46% lower risk of eosinophilic oesophagitis (EoE) and oesophageal eosinophilia in individuals infected with Helicobacter pylori [1]. While we commend the authors for their contributions, the decision to group EoE and oesophageal eosinophilia may have introduced bias, as these entities have dissimilar diagnostic criteria. According to the most recent clinical guideline, EoE can be diagnosed in the setting of symptoms of oesophageal dysfunction that are absent in oesophageal eosinophilia, plus an eosinophil-predominant infiltrate in the oesophagus [2].

The presence of oesophageal dysfunction is of primary importance in the diagnosis of EoE, especially since oesophageal eosinophilia (> 15 eosinophils per high-power field) can be found in up to 1.1% of the general population [3]. Consequently, oesophageal eosinophilia on routine biopsies may be incidental, as in other conditions [2, 3]. Oesophageal eosinophilia alone is a histological feature that does not constitute a diagnosis of EoE. These conditions should be analysed separately [4].

In the present meta-analysis, only 9 out of 19 studies employed a diagnostic definition consistent with current consensus criteria for EoE. Six studies included patients with oesophageal eosinophilia alone, three enrolled mixed populations and one did not specify the criteria used to define EoE or oesophageal eosinophilia. This heterogeneity in case definition may have introduced a significant risk of misclassification bias. Adopting more rigorous inclusion criteria, along with subgroup analyses based on clearly defined diagnostic categories, would have enhanced the accuracy and interpretability of the findings, thereby clarifying the actual impact of H. pylori infection on EoE. Notably, oesophageal eosinophilia can be asymptomatic or can present with non-specific symptoms that overlap with other oesophageal disorders, such as gastro-oesophageal reflux disease. In some cases, it may not necessitate specific treatment beyond clinical surveillance [5].

Moreover, the analysis revealed significant heterogeneity among included studies, especially when comparing the incidence of EoE in patients exposed to H. pylori versus those unexposed. This suggests that the results should be interpreted cautiously.

Finally, the data collected did not allow for a distinction between current and past H. pylori infection in most studies. Consequently, the analysis could not evaluate the impact of eradication therapies on the association between H. pylori and EoE, which is an important factor in understanding the relationship.

The meta-analysis highlights the need for future longitudinal and mechanistic studies, detailed subgroup analyses, evaluation of eradication therapy effects, and ongoing surveillance of H. pylori prevalence better to elucidate the nature and implications of their inverse relationship.

Fernanda Cristofori: conceptualization, validation, writing – original draft. Vanessa Nadia Dargenio: data curation, visualization, writing – original draft. Ruggiero Francavilla: conceptualization, validation, writing – review and editing.

The authors declare no conflicts of interest.

This article is linked to Spinelli et al. papers. To view this article, visit https://doi.org/10.1111/apt.70042 and https://doi.org/10.1111/apt.70204.