Objectives: Helicobacter pylori (H. pylon) infection seems to induce antralization (ie., gastric mucosal transformation from transitional or body type to antral type), which is strongly associated with gastric atrophy and intestinal metaplasia. The aim of this study was to determine the topographic associations of Ki-67 (a protein expressed in proliferative cells), Bax (a pro-apoptotic protein), and Bcl-2 (an antiapoptotic protein) expression with antralization.
Methods: In each of 104 patients, eight biopsy specimens were taken from the gastric antrum, incisura, body, and fundus for the determination of H. pylori infection, histological changes, and epithelial expression of Ki-67, Bax, and Bcl-2. A labeling index (LI), i.e., the rate of positive cells over total cells counted, was used for Ki-67 and Bax expression. Bcl-2 overexpression was considered to be present if the rate of Bcl-2 positive cells over total cells counted was > or = 5%.
Results: H. pylori infection was present at the gastric antrum, incisura, body, and fundus in 50, 48, 51, and 49 patients, respectively. Ki-67 LI was greater in the presence vs absence) of H. pylori infection at the antrum (51 vs 40), incisura (47 vs 36), body (43 vs 30), and fundus (41 vs 31) (all p < 0.001). At the incisura, Ki-67 LI was greater (47 vs 32, p < 0.001), Bax LI was lower (22 vs 30, p < 0.05), and prevalence of Bcl-2 overexpression was higher (44% vs 18%, p < 0.001) in the presence (vs absence) of antralization. Compared with normal mucosa, gastric atrophy/intestinal metaplasia were associated with an increased Ki-67 LI and decreased Bax LI at the antrum (49 vs 32 and 15 vs 23, respectively), incisura (47 vs 32 and 15 vs 26, respectively) (all p < 0.001). Bcl-2 overexpression was more frequent in gastric atrophy/intestinal metaplasia at the antrum (56% vs 11%, p < 0.001) and incisura (63% vs 19%, p < 0.001) compared with normal mucosa.
Conclusions: Antralization at the incisura is topographically associated with increased cell proliferation, reduced Bax expression, and Bcl-2 overexpression, which implies that antralization may be an important histological marker for future cancer risk.