Characterization of gastric mucosal lesions in patients with celiac disease: A prospective controlled study

OBJECTIVE: Several studies have demonstrated that chronic exposure to glute n may damage the structure and function of the gastric mucosa in gluten-sen sitive patients. However, until now, these abnormalities have been incomple tely studied. Our purpose in the present study was to characterize, in a pr ospective controlled study, the endoscopic and histological appearance of t he gastric mucosa in a large cohort of patients with celiac disease with an d without Helicobacter pylori (H. pylori) infection. METHODS: We evaluated biopsy specimens taken from the gastric body and antr um of 218 individuals who underwent upper endoscopy for small bowel biopsy. One hundred-four patients had celiac disease (80 of them at the time of di agnosis-untreated). In 114 subjects celiac disease was excluded. RESULTS: Endoscopic findings did not show a difference between the groups. The prevalence of cases with normal gastric mucosa, chronic superficial gas tritis, and atrophic gastritis was similar in patients and controls. Simila rly, presence of metaplasia, inflammatory activity, and lymphoid follicles and aggregates did not show differences between the groups. Histological or serological evidence of H. pylori infection was detected in 86% of patient s (82% of untreated celiacs and 95% of those on those taking treatment). Th e infection was highly prevalent in patients (89%) and controls (97%) diagn osed with chronic gastritis. Untreated patients had a significant greater I EL count in the antrum and corpus than controls (p < 0.0001 and p < 0.001, respectively). A global analysis of the data on intraepithelial lymphocyte (IEL) counts in the different populations suggest that the inflammatory sta te may represent the cumulative effect of H. pylori infection and gluten se nsitivity. Only three patients had TEL infiltration compatible with diagnos is of lymphocytic gastritis (count >25%) and three other patients had borde rline counts. CONCLUSIONS: According to our results, celiac disease patients presented a similar prevalence of gastric mucosal abnormalities compared with the contr ol population. Evidence of H. pylori infection was very high compared with the prevalence in the general Argentine population. As a particular observa tion in our celiac population, the disease was rarely associated with lymph ocytic gastritis. We suggest that the chronic inflammatory state evidenced by a gastric mucosal lymphocyte infiltration may be secondary to the combin ation of H. pylori infection and chronic gluten ingestion in gluten-sensiti ve subjects. (C) 1999 by Am. Cell. of Gastroenterology.