Histopathologic Analysis of Helicobacter Pylori Associated Gastritis.
- Author:
Ho Jung LEE
;
Eun Sil YU
;
In Chul LEE
- Publication Type:Original Article
- Keywords:
Helicobacter pylori;
Gastritis;
Histopathological analysis
- MeSH:
Biopsy
- From:Korean Journal of Pathology
1996;30(9):764-774
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Gastric mucosa shows continuous changes in surface epithelium as well as inflammatory reaction by various substances from the outside and their metabolic products. Gastric mucosal lesions are proven to be associated with bacterial infection by the discovery of Heliobacter pylori(H. pylori) and many studies about histopathologic changes of gastric mucosa associated H. pylori infection has been advanced. It is known that H. pylori associated gastritis displays surface foveolar epithelial changes, such as cytoplasmic vacuolation, mucin loss, juxtaluminal cytoplasm erosion, epithelial denudation, and mucosal irregularity. There have been many studies that H. pylori infection is associated with intestinal metaplasia, gastric dysplasia, and carcinoma. Also chronic H. pylori infection with its induction of gastric lymphoid follicle has been implicated as a precursor of gastric lymphoma of the unique B-cell type that arises from mucosa-associated lymphoid tissue(MALT). However, these gastric mucosal changes are also observed in gastritis with other causes. In this study, we aimed to define specific histopathiologic findings associated with H. pylori infection. A total of 463 gastric biopsy specimens were reviewed. They were Helicobacter-associated gastritis and were divided as many (MH), a few (AH), and no (NH), according to the number of H. pylori. 210 (MH), 131 (AH), and 122 (NH) biopsy specimens were included. Lymphocytes, plasma cells in lamina propria, eosinophils and neutrophils in surface epithelium and crypt as well as lamina propria were graded from 0 to 3. Surface epithelial changes including cytoplasmic vacuolation, mucin loss, juxtaluminal erosion, epithelial denudation and mucosal irregrarity were observed in 200 of 210 cases(95%) in MH group, 34 of 131 cases(26%) in AH group, and 6 of 122 cases(5%) in NH group. This result indicates there is significant difference in surface epithelial changes according to the number of H. pylori(p<0.001). Severity of eosinophil, neutrophil, lymphocyte, and plasma cell infiltration is increased in proportion to the number of H. pylori. Especially, neutrophilic infiltration is not identified in 95 of 122 cases(78%) in NH group, whereas MH group shows severe infitration (grade 3) in 127 of 210 cases(61%), and no (grade 0) in 11 of 210 cases(5%). This data well explains that the severity of neutrophil infiltration is associated with, the degree of H. pylori infection in chronic active gastritis, with statistical significance. The prevalence of lymphoid follicle formation was 17 of 120 cases(14%) in NH group, 24 of 131 cases(18%) in AH group, and 52 of 210 cases(25%) in MH group. This shows that lymphoid follicle formation correlates with the number of H. pylori, but without statistical significance. The prevalence of intestinal metaplasia in NH, AH, and MH was 43 of 122 cases(35%), 46 of 131 cases(35%), and 69 of 210 cases(33%), showing no association between intestinal metaplasia and H. pylori. In summary, H. pylori associated gastritis dispays characteristic histopathological changes in gastric mucosa, in which surface epithelial changes and various inflammatory infiltrates are increased in proportion to the number of H. pylori. Especially vacuolization of surface foveolar epithelium, cryptitis, and crypt abscess are specific findings of H. pylori associated gastritis.
