Eosinophilic oesophagitis (EoO) is an immune-mediated disease characterised by symptoms of oesophageal dysfunction (mainly dysphagia), endoscopic abnormalities of the oesophageal mucosa and an infiltrate of eosinophils in the oesophageal mucosa with a density greater than 15 eosinophils per high-power field (eos/HPF).1 It is a chronic, progressive, relapsing disease affecting children and adults. In the former it usually presents as an inflammatory phenotype of the oesophagus and in adults as a fibrostenotic phenotype, characterised by fibrosis and oesophageal stricture resulting in food impaction.2 To diagnose EoO, other causes of oesophageal eosinophilia must be ruled out.

EoO was first described by Landres et al. in 19783 in a patient with vigorous achalasia, but it was not until 1993 that it was recognised as a specific pathological condition of the oesophagus.4 The prevalence of EoO is not evenly distributed around the world. It is most prevalent in northern European countries and Spain, as well as in forested areas with temperate climates in the USA, Canada and Australia, while it is less common in countries in Latin America, Asia and Africa.5 In the countries where it is most typically found, its incidence and prevalence has doubled in the last three decades, leading to it being described as an epidemic.6, 7 The causes of this increased incidence are unknown.

In essence, EoO is an allergic condition, mediated primarily by a Th2-type immune response involving eosinophils, mast cells and chemical mediators such as eotaxin-3, interleukin (IL)-4, IL-5 and IL-13.7 Triggers for the disease are usually environmental and food allergens. Some 40%–60% of patients with EoO have a history of atopy.8 However, the reasons why people in these geographical regions used to tolerate these allergens and now react in this way are unknown. It has been proposed that improved social and economic conditions in industrialised countries have resulted in changes in the habits of the population, based on better hygienic conditions, leading to an increase in allergic conditions mediated by the Th2 immune response.9

Helicobacter pylori (H. pylori) is a Gram-negative bacterium that causes the most common chronic infection globally. Its prevalence is very uneven in different regions of the world. The extent of its prevalence is in most cases closely correlated with the socio-economic status of the population, and it is much more prevalent in underdeveloped countries.10H. pylori infection is usually acquired in childhood and is associated with peptic ulcer disease and gastric adenocarcinoma.11

In recent years, several studies, mostly case-control studies, have been published describing an inverse relationship between the prevalence of EoO and H. pylori infection, which may represent a “protective effect” conferred by the infection. A recent meta-analysis of 11 studies reported a 37% reduction in the risk of EoO in patients with H. pylori infection.12 However, a prospective trial by Molina-Infante et al. found no significant inverse association between H. pylori and EoO, casting doubt on this relationship.13 The difference in the results of these studies may be due to methodological differences. In addition, most of the studies have been conducted in Europe, the USA and Australia, where the prevalence of H. pylori is low. To date, no trials have been conducted in Latin America where the prevalence of H. pylori is very high. In light of the above, we conducted a study to assess the type of relationship between H. pylori infection and EoO in Mexican patients.