Objective. Helicobacter pylori infection is the major agent of gastric damage. Coeliac disease may affect the morphology and function of the entire gastrointestinal tract from the stomach to the colon. The aim of this study was to assess the gastric histological pattern in patients with H. pylori and untreated celiac disease. Material and methods. We retrospectively enrolled 183 H. pylori-positive patients with (85, group A) and without (98, group B) untreated coeliac disease. The groups were similar for age, gender and smoking habit, and all the patients came from the same geographical area. Histological evaluation of gastric pattern was performed on 4 biopsies (2 in the antrum, 2 in the corpus). Gastric damage was classified according to the modified Sydney System. Diagnosis of H. pylori infection was based on positivity to histology. The chisquare test was used to assess differences between groups. A p-value < 0.05 was considered significant. Results. Group A showed a significantly higher prevalence of follicular gastritis than group B (23.5%versus 12.2%, p = 0.045). A significantly lower prevalence of atrophic gastritis was observed in group A compared with that in group B (6%versus 22.5%, p = 0.002). The prevalenceof chronic superficial gastritis, activity degree and intestinal metaplasia was similar between the two groups. Conclusions. In patients with H. pylori infection, untreated coeliac disease could represent a risk factor for follicular gastritis and is associated with a lower prevalence of atrophic gastritis. The complex interaction between H. pylori and untreated coeliac disease on Th-1/Th-2 balance in the gastric mucosa could explain these results. Objectives of this study was to assess the gastric histological pattern in patients with H. pylori and untreated celiac disease. Material and methods. We retrospectively enrolled 183 H. pylori-positive patients with (85, group A) and without (98, group B) untreated coeliac disease. The groups were similar for age, gender and smoking habit , and all the patients came from the same geographical area. Histological evaluation of gastric pattern was performed on 4 biopsies (2 in the antrum, 2 in the corpus). Gastric damage was classified according to the modified Sydney System. Diagnosis of H. pylori infection was based on positivity to histology. The chisquare test was used to assess differences between groups. A p-value <0.05 was considered significant. Results. Group A showed a significantly A prevalence of follicular gastritis than group B (23.5% versus 12.2%, p = 0.045). A significant lower prevalence of atrophic gastritis was observed in group A compared with that in group B (6% versus 22.5%, p = 0.002). The prevalence of chronic superficial gastritis, activity degree and intestinal metaplasia was similar between the two groups. Conclusions. In patients with H. pylori infection, untreated coeliac disease could represent a risk factor for follicular gastritis and is associated with a lower prevalence of atrophic gastritis. The complex interaction between H. pylori and untreated coeliac disease on Th-1 / Th-2 balance in the gastric mucosa could explain these results.