Biomedical subjects
Jenny Ma Wyatt
Publications and source records attributed to Jenny Ma Wyatt.
Antralization of gastric incisura is topographically associated with increased gastric epithelial apoptosis and proliferation, but not with CagA seropositivity.
BACKGROUND AND AIMS: Helicobacter pylori infection is linked with increased antralization at the gastric incisura. The present study aimed to determine if antralization is associated with altered gastric epithelial apoptosis and proliferation and with seropositivity of the cytotoxin-associated gene product A (CagA) of H. pylori. METHODS: Gastric biopsies taken from the antrum, incisura, body and fundus of 75 patients (34 male, 41 female; mean age 59.5 years) were used for diagnosis of H. pylori infection and assessments of histological changes. Apoptosis and Ki-67 expression in epithelial cells were determined for the antral, incisura and body biopsies by immunohistochemistry. Serum samples were tested by enzyme-linked immunosorbent assays for anti-H. pylori and anti-CagA IgG antibodies. RESULTS: Apoptotic index (AI) and Ki-67 proliferation index (PI) were greater in the presence (vs absence) of H. pylori infection at the antrum, incisura and body (all P < 0.001), and topographically associated with chronic gastritis and gastric atrophy/intestinal metaplasia at the antrum and incisura (all P < 0.001). Moreover, AI and PI were greater in the presence (vs absence) of antralization at the incisura (20.2 +/- 0.9 vs 11.4 +/- 0.1.1 and 48.9 +/- 2.5 vs 29.9 +/- 2.5, both P < 0.001). CagA seroprevalence was 41% in the 39 infected patients. CagA seropositivity was associated with gastric atrophy/intestinal metaplasia at the antrum (chi(2) = 4.67, P = 0.03) and incisura (chi(2) = 4.88, P = 0.03), but not associated with gastric epithelial apoptosis and Ki-67 expression, nor with antralization at the incisura. CONCLUSIONS: Antralization of gastric incisura is topographically associated with increased gastric epithelial apoptosis and proliferation, but not with CagA seropositivity.
Topographic association of gastric epithelial expression of Ki-67, Bax, and Bcl-2 with antralization in the gastric incisura, body, and fundus.
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.