Antral-type mucosa in the gastric incisura, body, and fundus (antralization): A link between Helicobacter pylori infection and intestinal metaplasia?

OBJECTIVES: Helicobacter pylori is a carcinogen; gastric carcinoma involves a multistep process from chronic gastritis to atrophy, intestinal metaplas ia, and dysplasia. The aims of this study were to determine the types of mu cosa at different gastric sites in H. pylori-infected and uninfected patien ts, and whether the presence of antral-type mucosa in the incisura, body, a nd fundus is associated with gastric atrophy and intestinal metaplasia. METHODS: Two hundred and sixty-eight patients with dyspepsia were enrolled. Eight biopsies (i.e., antrum x3, body x2, fundus x2, and incisura x1) were obtained. One antral biopsy was used for the CLO-test. Three (each from th e antrum, body, and fundus) were cultured. The remaining biopsies were exam ined histologically according to the updated Sydney System after staining w ith hematoxylin and eosin and Giemsa. A validated serological test was also applied. RESULTS: Overall, 113 (42%) patients were infected with H. pylori. At the i ncisura, antral-type mucosa was more prevalent in infected than in uninfect ed patients (84% vs 18%; odds ratio [OR] = 23.9, 95% confidence interval [C I] 12.5-45.8; p < 0.001). Atrophic gastritis and intestinal metaplasia at t he incisura was present in 19.5% and 13.3%, respectively, of infected, and 4.5% and 3.2%, respectively, of uninfected patients (both p < 0.01). Moreov er, atrophic gastritis at the incisura was associated with the presence of antral-type mucosa at the site (termed antralization); the prevalence of at rophic gastritis was 19.5% (24/123) in the presence of antralization. where as the rate was 2.1% (3/145) without antralization (OR = 11.4, 95% CI 3.4-3 9.2; p < 0.001). Similarly, at the incisura, 16.3% (20/123) of "antralized" cases and 1.4% (2/145) of "unantralized" cases had intestinal metaplasia ( OR = 13.8, 95% CI, 3.2-60.7; p ( 0.001). The association between antralizat ion at gastric body and fundus also appeared to be associated with atrophic gastritis and intestinal metaplasia at these sites. CONCLUSIONS: Atrophic gastritis and intestinal metaplasia occurs predominan tly at the gastric antrum and incisura with H. pylori infection. Antralizat ion of the gastric incisura is a common event in H. pylori-infected patient s, and appears to be associated with an increased risk of atrophic gastriti s and intestinal metaplasia.