Both lymphocytic gastritis and gastric mucosa associated lymphoid tissue (MALT) lymphoma are associated with Helicobacter pylori (H. pylori) infection. However, this association has not been fully elucidated. We report two cases of lymphocytic gastritis in 57-year-old male and 47-year-old female patients which were diagnosed after the H. pylori eradication to treat gastric MALT lymphoma. MALT lymphoma was successfully treated in case 1, but residual MALT lymphoma remained in case 2. During the follow-up endoscopic examinations, several elevated erosions in case 1 and irregular mucosal atrophy in case 2 were newly detected. Biopsy specimens showed marked infiltration of lymphocytes in the surface epithelium (56.6+/-15.9 intraepithelial lymphocytes (IELs)/100 epithelial cells in case 1 and 40.5+/-9.3 IELs/100 epithelial cells in case 2), which were exclusively CD8-positive T lymphocytes. These findings suggest that H. pylori infection may cause a monoclonal proliferation of B lymphocytes, leading to MALT lymphoma as well as polyclonal proliferation of T lymphocytes which subsequently infiltrated into the surface epithelium as a host immune reaction, resulting in lymphocytic gastritis.
Gastric Mucosa/*pathology ; Gastritis/*complications/microbiology/pathology ; Helicobacter Infections/*complications ; *Helicobacter pylori ; Humans ; Lymphocytes/*pathology ; Lymphoma, B-Cell, Marginal Zone/*complications/microbiology ; Male ; Middle Aged ; Stomach Neoplasms/*complications

No abstract availble.
Adult ; Gastric Mucosa/*pathology ; Gastritis, Hypertrophic/microbiology/*pathology ; Gastroscopy ; Helicobacter Infections/complications/*drug therapy ; *Helicobacter pylori ; Humans ; Male

BACKGROUND/AIMS: Helicobacter pylori (H. pylori) infection can lead to gastric adenoma and carcinoma through atrophic gastritis and intestinal metaplasia. Imbalance between apoptosis and proliferation may play a role in gastric carcinogenesis. We tried to investigate H. pylori infection rate, grade of gastritis, environmental risk factors, expression rate of apoptosis and cell proliferation in mucosa adjacent to tumor, and we also tried to find significant factors associated with gastric carcinogenesis. METHODS: Endoscopically diagnosed twenty cases of intestinal type gastric carcinoma, 20 cases of gastric adenoma, and 40 cases of control (normal or gastritis) were enrolled. H. pylori infection rate, histologic grading, apoptosis and immunohistochemical stain (Ki-67 and p53) to check mucosal proliferation were done in endoscopically biopsied tissues at antrum and body at least 2 cm apart from adenoma or carcinoma. RESULTS: In three groups, H. pylori infection rates were not significantly different. In the multivariate analysis, only atrophy of gland was a significant risk factor for adenoma compared to control group (OR 3.7). Intestinal metaplasia in antrum and alcohol drinking were significant risk factors for carcinoma compared to control group (OR 4.4 and 4.9 respectively). Expressions of apoptosis, Ki-67 and p53 were not significantly different in three groups. CONCLUSIONS: Intestinal metaplasia in antrum and alcohol drinking are significant risk factors for gastric carcinoma. Degree of mucosal proliferation and apoptosis in gastric mucosa adjacent to tumor are not significantly different in three groups.
Adenocarcinoma/microbiology/*pathology ; Adenoma/microbiology/*pathology ; Adult ; Aged ; Aged, 80 and over ; *Apoptosis ; *Cell Proliferation ; English Abstract ; Female ; Gastric Mucosa/*pathology ; Gastritis/microbiology/pathology ; Helicobacter Infections/complications/pathology ; Helicobacter pylori ; Humans ; Male ; Middle Aged ; Risk Factors ; Stomach Neoplasms/microbiology/*pathology

BACKGROUND: To assess the relationships among gastric pH and ammonia level, H. pylori infection, and gastric mucosal histology, we determined the gastric juice pH and ammonia concentration in H. pylori gastritis. METHODS: The pH levels and ammonia concentrations were determined in gastric juice collected from 143 patients with dyspepsia during an endoscopy and compared according to a H. pylori infection. We also looked for correlations between two chemical parameters, between each of these parameters and H. pylori density, and histology. RESULTS: Gastric pH levels and ammonia concentrations were higher in 94 infected patients than in the uninfected (3.16 vs. 1.55, p=0.0001; 5.58 +/- 2.69 vs. 2.00 +/- 1.49 moL/L, p=0.0001). Among 28 patients who received eradication therapy, 19 (67.9%) were successful, and their gastric pH levels and ammonia concentrations were significantly lower than those in the eradication failure group (1.60 vs. 2.33, p=0.007; 1.77 +/- 1.28 vs. 4.02 +/- 1.20 micro moL/L, p=0.0001). Gastric pH was significantly associated with intragastric ammonia concentration (p=0.025) and gastritis activity (p=0.018). Gastric pH and the ammonia level were significantly correlated with each other (rs=0.495, p< 0.01), and with H. pylori density (rs=0.467; rs=0.735, p< 0.01), gastritis severity (rs=0.343; rs=0.478, p< 0.01), and gastritis activity (rs=0.418; rs=0.579, p< 0.01). CONCLUSION: Gastric juice pH and ammonia concentration reflect well the status of a H. pylori infection, and significantly correlate with each other and with H. pylori density, gastritis severity and activity. These findings suggest that intragastric ammonia produced by H. pylori may have a partial role in an increased gastric juice pH, and has a pathogenic role in H. pylori gastritis.
Adult ; Aged ; Ammonia/*analysis ; Female ; Gastric Juice/*chemistry ; Gastric Mucosa/*pathology ; Gastritis/*microbiology ; Helicobacter Infections/*complications ; Humans ; Hydrogen-Ion Concentration ; Male ; Middle Aged ; Severity of Illness Index

Animals ; Anti-Bacterial Agents ; administration & dosage ; Escherichia coli ; Female ; Galactosylceramides ; immunology ; Gastric Mucosa ; pathology ; Gastritis, Atrophic ; pathology ; Helicobacter Infections ; complications ; drug therapy ; Helicobacter pylori ; pathogenicity ; Humans ; Inflammation ; pathology ; Intestines ; microbiology ; Levofloxacin ; Lymphocyte Activation ; Male ; Natural Killer T-Cells ; microbiology ; Ofloxacin ; administration & dosage ; Sphingomonas ; Stomach ; pathology

BACKGROUND/AIMS: Long-term Helicobater pylori infection results in atrophic gastritis and intestinal metaplasia, and increases the risk of gastric cancer. However, it is still controversial that eradication of H. pylori improves atrophy or metaplasia. Therefore, we investigated histological changes after the H. pylori eradication in patients with atrophy or metaplasia. METHODS: One hundred seven patients who received successful eradication of H. pylori infection in Hanyang University, Guri Hospital from March 2001 to April 2006, were enrolled. Antral biopsy was taken before the eradication to confirm the H. pylori infection and grade of atrophy or metaplasia by updated Sydney System. After a certain period of time, antral biopsy was repeatedly taken to confirm the eradication and investigate histological changes of atrophy or metaplasia. RESULTS: Mean age of the patients was 55.3+/-11.3, and average follow-up period was 28.7+/-13.9 months. Endoscopic diagnosis included gastric ulcer, duodenal ulcer, non-ulcer antral gastritis. Atrophy was observed in 41 of 91 and their average score was 0.73+/-0.92. After the eradication of H. pylori, atrophy was improved (0.38+/-0.70, p=0.025). However, metaplasia which was observed in 49 of 107, did not significantly improve during the follow-up period. Newly developed atrophy (7 of 38) or metaplasia (18 of 49) was observed in patients who without atrophy or metaplasia initially. Their average scores were slightly lower than those of cases with pre-existing atrophy or metaplasia without statistical significance. CONCLUSIONS: After the eradication of H. pylori infection, atrophic gastritis may be improved, but change of intestinal metaplasia is milder and may take longer duration for improvement.
Adult ; Aged ; Anti-Bacterial Agents/therapeutic use ; Anti-Ulcer Agents/therapeutic use ; Data Interpretation, Statistical ; Female ; Follow-Up Studies ; Gastritis, Atrophic/etiology/microbiology/*pathology ; Helicobacter Infections/*complications/drug therapy ; *Helicobacter pylori/drug effects/isolation & purification ; Humans ; Intestines/*pathology ; Male ; Metaplasia/microbiology ; Middle Aged ; Time Factors

BACKGROUND/AIMS: Helicobacter pylori infection is linked to the development of gastric cancer. H. pylori-associated gastric inflammation is considered to be the first important step in the histogenesis of such neoplasia. However, studies that compare proteome of gastric mucosa infected with or without H. pylori are lacking. METHODS: We employed proteomics analysis on the endoscopic biopsy specimens of gastric mucosa obtained from two groups (30 cases): healthy subjects without H. pylori infection (15 cases), and gastritis patients with H. pylori infection (15 cases). The pooled proteins obtained from gastric mucosa infected with or without H. pylori were separated by two-dimensional gel electrophoresis and analyzed by a computer-aided program. The altered protein expressions were then identified by mass spectrometry and validated by Western blotting and immunohistochemistry. RESULTS: On mass spectrometry using MALDI TOF(TM) Analyzer, the up-regulation of Keratin 1, ezrin, adenosine triphosphate (ATP) synthase subunit alpha mitochondrial isoform c, Keratin type I cytoskeletal 19, and Keratin type I cytoskeletal 9 were identified; in contrast, 71 kd heat shock cognate protein, ATP synthase subunit alpha mitochondrial precursor, and annexin IV were down-regulated. Among them, membrane cytoskeleton linker ezrin was validated using Western blot and immunohistochemistry. CONCLUSIONS: Expression of ezrin was significantly different between the gastric mucosa with and without H. pylori infection. Therefore, ezrin could be considered a promising potential molecular marker for detecting H. pylori infection in gastric mucosa.
Blotting, Western ; Cytoskeletal Proteins/metabolism ; Down-Regulation ; Electrophoresis, Gel, Two-Dimensional ; Female ; Gastric Mucosa/*metabolism/microbiology ; Gastritis/complications/metabolism/pathology ; Gastroscopy ; Helicobacter Infections/complications/metabolism/*pathology ; *Helicobacter pylori ; Humans ; Immunohistochemistry ; Male ; Proteome/*analysis ; *Proteomics ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; Up-Regulation

It is often difficult to differentiate gastric mucosa-associated lymphoid tissue (MALT) lymphoma from Helicobacter pylori-associated follicular gastritis, and thus, it becomes unclear how to manage these diseases. This study aimed to explore the management strategy for and the long-term outcomes of suspicious gastric MALT lymphoma detected by forceps biopsy during screening upper endoscopy. Between October 2003 and May 2013, consecutive subjects who were diagnosed with suspicious gastric MALT lymphomas by screening endoscopy in a health checkup program in Korea were retrospectively enrolled. Suspicious MALT lymphoma was defined as a Wotherspoon score of 3 or 4 upon pathological evaluation of the biopsy specimen. Of 105,164 subjects who underwent screening endoscopies, 49 patients with suspicious MALT lymphomas who underwent subsequent endoscopy were enrolled. Eight patients received a subsequent endoscopy without H. pylori eradication (subsequent endoscopy only group), and 41 patients received H. pylori eradication first followed by endoscopy (eradication first group). MALT lymphoma development was significantly lower in the eradication first group (2/41, 4.9%) than in the subsequent endoscopy only group (3/8, 37.5%, P = 0.026). Notably, among 35 patients with successful H. pylori eradication, there was only one MALT lymphoma patient (2.9%) in whom complete remission was achieved, and there was no recurrence during a median 45 months of endoscopic follow-up. H. pylori eradication with subsequent endoscopy would be a practical management option for suspicious MALT lymphoma detected in a forceps biopsy specimen obtained during screening upper endoscopy.
Adult ; Aged ; Anti-Bacterial Agents/therapeutic use ; Biopsy ; Female ; Follow-Up Studies ; Gastric Mucosa/*pathology ; Gastritis/diagnosis/etiology/microbiology ; Gastroscopy ; Helicobacter Infections/complications/*diagnosis/drug therapy ; Humans ; Lymphoma, B-Cell, Marginal Zone/complications/*diagnosis/pathology ; Male ; Middle Aged ; Republic of Korea ; Retrospective Studies

OBJECTIVETo establish an animal model of gastric cancer by long-term infection of Helicobacter pylori (H.pylori) and to elucidate the pathogenesis by proteomics analysis.

METHODSFifty male Mongolian gerbils (4-5 week-old and weighted 60-100 g) were infected with H.pylori and the gastric tissues were obtained after the infection at 3, 6, 12 and 24 months. Histological changes were evaluated by H-E staining of the gastric tissue sections. Detection of H.pylori was performed by in-vitro culture of fresh gastric tissue samples, PCR amplification of H.pylori 16s rRNA and localization by silver staining. In addition, proteins extracted from gastric tissue samples were subjected to two-dimensional electrophoresis (2-DE) at various infection time points. Protein spots with increased quantity over the course of H.pylori infection were selected and analyzed by LC-MS/MS. Finally, differentially expressed proteins between human gastric cancer tissue samples and lymph nodes were analyzed by real-time RT-PCR.

RESULTSColonization of H.pylori was observed in gastric tissue of gerbils as early as 3 months after H.pylori infection, and persisted till 24 months. Pathological examination of infected animals showed various histological changes including acute gastritis, atrophic gastritis, intestinal metaplasia and gastric carcinoma. Seventy-eight differentially expressed proteins were identified by proteomics analysis, among which 36 proteins were up-regulated and 42 were down-regulated. Analyzed by LC-MS/MS, ten proteins were identified, including lactate dehydrogenase, ATP synthase, fatty acid-binding protein, COX5B, peroxiredoxin-4, peroxide reductase, transgelin, succinyl-CoA ligase, keratin and protein disulfide-isomerase A2, among which transgelin, ATP synthase and lactate dehydrogenase were highly expressed in human gastric carcinoma and lymph nodes.

CONCLUSIONSH.pylori infection induces the expression of transgelin, ATP synthase and lactate dehydrogenase, implying possible roles in the pathogenesis of gastric diseases including cancer.

Animals ; Disease Models, Animal ; Gastritis ; microbiology ; pathology ; Gerbillinae ; Helicobacter Infections ; complications ; metabolism ; Helicobacter pylori ; genetics ; Humans ; L-Lactate Dehydrogenase ; metabolism ; Male ; Metaplasia ; Microfilament Proteins ; metabolism ; Muscle Proteins ; metabolism ; Proteomics ; Proton-Translocating ATPases ; metabolism ; RNA, Ribosomal, 16S ; analysis ; Stomach Neoplasms ; metabolism ; microbiology ; Tandem Mass Spectrometry