Relationship between the Hp infection and its carcinogenic factor to gastric carcinoma
Wang Li
Abstract
Wang Li
Abstract
Objective: To define relationship between Helicobacter pylori (Hp) and gastric carcinoma on its carcinogenicity in order to use antibiotic treatment to Hp infection for preventing early gastric carcinoma. Methods: 129 patients with peptic ulcer, 315 patients with chronic gastritis, and 97 patients with gastric carcinoma were diagnosed by endscopy and pathological means with hemoloxylin-eosin staining. All patient′s biospy specimens from the gastric antrum mucosa were examined by Warthin-Starry silver staining, mucosa smear gram-staining,urease test, and polymerase chain reaction (PCR) to find Hp. Proliferating cell nuclear antigen (PCNA) and p53 protein were detected in the active chronic gastritis and gastric carcinoma (20 patients) respectively by immunohistochemistry (LSAB). Results: (1) Hp infectious rate of the active chronic gastritis was significantly higher than that of the non-active chronic gastritis, 76.0%, 47.1%(P0.05)respectively. (2) Hp infectious rate showed significant difference in the light, mild, and serious chronic gastritis, 40.5%?72.7%?86.7% (P0.05) respectively. (3) Hp was found in 91 (70.5%) out of 129 patients with peptic ulcer, in 192(60.9%) out of 315 patients with chronic gastritis, and in 56(57.7%) out of 97 patients with gastric carcinoma. Hp infectious rate had no significant difference in three groups (P0.05). (4) p53 protein positive rate in gastric carcinoma was 80.0%; active chronic gastritis was negative (P0.05). (5) In chronic gastritis and carcinoma, PCNA positive rates were 85.0% and 95.0% (P0.05) respectively. Conclusion: Hp infection may result in gastric carcinoma by epithelium metaplasia.
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Objective: To define relationship between Helicobacter pylori (Hp) and gastric carcinoma on its carcinogenicity in order to use antibiotic treatment to Hp infection for preventing early gastric carcinoma. Methods: 129 patients with peptic ulcer, 315 patients with chronic gastritis, and 97 patients with gastric carcinoma were diagnosed by endscopy and pathological means with hemoloxylin-eosin staining. All patient′s biospy specimens from the gastric antrum mucosa were examined by Warthin-Starry silver staining, mucosa smear gram-staining,urease test, and polymerase chain reaction (PCR) to find Hp. Proliferating cell nuclear antigen (PCNA) and p53 protein were detected in the active chronic gastritis and gastric carcinoma (20 patients) respectively by immunohistochemistry (LSAB). Results: (1) Hp infectious rate of the active chronic gastritis was significantly higher than that of the non-active chronic gastritis, 76.0%, 47.1%(P0.05)respectively. (2) Hp infectious rate showed significant difference in the light, mild, and serious chronic gastritis, 40.5%?72.7%?86.7% (P0.05) respectively. (3) Hp was found in 91 (70.5%) out of 129 patients with peptic ulcer, in 192(60.9%) out of 315 patients with chronic gastritis, and in 56(57.7%) out of 97 patients with gastric carcinoma. Hp infectious rate had no significant difference in three groups (P0.05). (4) p53 protein positive rate in gastric carcinoma was 80.0%; active chronic gastritis was negative (P0.05). (5) In chronic gastritis and carcinoma, PCNA positive rates were 85.0% and 95.0% (P0.05) respectively. Conclusion: Hp infection may result in gastric carcinoma by epithelium metaplasia.
Key concepts: Gastroenterology, Chronic gastritis, Medicine, Helicobacter pylori, Gastritis, Internal medicine, Rapid urease test, Atrophic gastritis