• Korean Journal of Clinical Laboratory Science
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• v.46 no.3
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• pp.91-98
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• 2014

Primary gastric lymphoma (PGL) is derived from mucosa-associated lymphoid tissue (MALT) and it differs from nodal lymphoma in histologic features and biologic behavior. Recent studies have showed that Helicobacter pylori (H.pylori ) infection is closely related to the development of low grade gastric lymphoma, and eradication of the infection induces regression of the tumor. H. pylori infection is known to be important to the development of gastric MALT lymphoma. The aim of this study was to elucidate the histopathological behavior of PGL according to the concept of MALT and to compare the predictive value of tests frequently used for diagnosis of H. pylori. The histological features of gastric lymphoma arising from MALT are the replacement of glands by uniform dense infiltration of centrocyte-like cells in the lamina propria and lymphoidepithelial lesion. H. pylori-associated histologic changes of neutrophilic infiltration, lymphoid follicle or aggregates formation and intestinal metaplasia, and H. pylori immunoreactivity were analyzed. Detection of H. pylori in chronic active gastritis and peptic ulcer suggests a possible role of H. pylori in the pathogenesis. Giemsa, Toluidine blue and Long H&E stains were used in H. pylori detection. Histopathological examination of gastric biopsy specimens revealed lymphoepithelial lesions pathognomonic of MALT lymphoma, and immunohistochemical staining for CD20 was diffusely positive. CD3 was positive in reactive T cells. PAX-5 was negative except the follicle. Bcl-2, cytokeratin, Ki-67, and c-myc were positive. The findings may indicate a predictable transition of low grade to high grade, and c-myc may be used as a valuable marker before molecular pathology diagnosis.

• Journal of Life Science
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• v.10 no.6
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• pp.630-639
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• 2000

The gastric pathogen Helicobacter pylori(H. pylori) establishes long-term chronic infection that can lead to atrophic gastritis, intestinal metaplasia, and gastric cancer. H. pylori, which express cytotoxic genes is now recohnized as a cause of peptic ulcer and is also a major risk factor for the development of gastric adenocarcinoma. We performed this study 1) to assess the detection rate of H. pylori according to direct investigation of bacteria of gastric biopsy specimen and two serologic tests of GAP test and Helico blot 2.0 system in the symptomatic and non-symptomatic group 2) to evaluate and compare the efficacy of two serologic tests of GAP test and Helico blot 2.0 system for the diagnosis of H. pylori infection. Forty-nine patients were positive for H pylori infection based on direct investigation of bacteria by histology. The detection rates of H. pylori infection based on direct investigation of bacteria by histology. The detection rates of H. phlori were significantly lower in gastric cancer than in other gastroduodenal disease(p<0.05). The concordance of two serologic tests of GAP test and Helico blot 2.0 system is poor. There was no statistically significant difference between the expression rate of CagA and VacA in the symptomatic and non-symptomatic group. Although Helico blot 2.0 system may not displace GAP test, it was a very sensitive serologic test for the diagnosis of H. pylori infection and it was used to detect IgG antibodies to H. pylori-specific antigens, including CagA, VacA and the various urease subunit. Our data suggest that further investigation is needed to determine whether or not the serologic expression of cytotoxic gene may be clinical usefulness of diagnostic methods in the gastroduodenal disease.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.5 no.1
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• pp.1-10
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• 2002

Purpose; Dysregulation of gastric epithelial cell proliferation and apoptosis are important in development of ulcer, atrophy and neoplasia in Helicobacter pylori (H. pylori) infection. The aim of this study was to investigate the effect of infection of H. pylori on gastric epithelial cell proliferation and apoptosis in children. Methods: Histological grading by updated Sydney system, PCNA immunostaining and TUNEL method were performed in H. pylori positive (N=58) and negative (N=40) gastric biopsy specimens. Results: In H. pylori positive children, there were significantly higher grade of polymorphonuclear neutrophil activity (P=0.000), chronic inflammation (P=0.000), epithelial damage (P=0.000) and lymphoid follicles (P=0.000) than in H. pylori negative children. Intestinal metaplasia was not seen in H. pylori positive children. PCNA index was significantly different between H. pylori positive children ($67.8{\pm}18.13$) and H. pylori negative children ($54.8{\pm}14.46$, P=0.000). There was positive correlation between PCNA index and H. pylori density (r=0.277, P=0.007), polymorphonuclear neutrophil activity (r=0.280, P=0.007) and chronic inflammation (r=0.284, P=0.006). Apoptosis index of H. pylori positive children ($0.44{\pm}0.447$) was significantly higher than of H. pylori negative children ($0.14{\pm}0.196$, P=0.000). There was positive correlation between apoptosis index and H. pylori density (r=0.472, P=0.000), polymorphonuclear neutrophil activity (r=0.370, P=0.001) and chronic inflammation (r=0.483, P=0.000). There was positive correlation between PCNA index and apoptosis index (r=0.353, P=0.003). Conclusion: The PCNA and apoptosis index in H. pylori positive children were significantly higher than in H. pylori negative children. This study suggested that gastric epithelial cell proliferation and apoptosis are important to pathogenesis of H. pylori infection in children.