Journal of gastroenterology and hepatology · 2004
Antralization of gastric incisura is topographically associated with increased gastric epithelial apoptosis and proliferation, but not with CagA seropositivity.
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Xia Harry Hua-Xiang, Wong Benjamin Chun-Yu, Zhang Gui-Shui, Yang Yi, Wyatt Jenny Ma, Adams Stuart, Cheung Karen, Lam Shiu Kum, Talley Nicholas J
Аннотация
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.
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.