The relationship between Helicobacter pylori (H. pylori) infection and gastro-esophageal reflux disease (GERD) is complex. Since some studies have suggested that H. pylori eradication may result in an increased incidence of GERD in duodenal ulcer patients, there have been debates about the protective function of H. pylori infection on GERD. H. pylori-associated antral gastritis can induce increased gastric acid output via increasing gastrin secretion. Changes in gastric acid secretion depend on the distribution (e.g. antral, corpus or pangastritis) or severity of gastritis, not on H. pylori infection itself. Patients with H. pylori infection are at risk of developing gastric mucosal atrophy, and a cohort study suggested that long-term proton pump inhibitor therapy for GERD may accelerate this process. Therefore, it has been recommended that H. pylori should be treated in GERD patients in whom a long-term antisecretory therapy is planned. The previous hypothesis that 'H. pylori infection protects from the development of GERD' is thought to be an erroneous concept recently.
Gastritis/microbiology ; Gastroesophageal Reflux/drug therapy/*microbiology ; Helicobacter Infections/*complications/drug therapy ; *Helicobacter pylori ; Humans

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

BACKGROUND/AIMS: This study was performed to evaluate whether the prevalence rates of primary antibiotic resistance in Helicobacter pylori (H. pylori) isolates and the eradication rate of H. pylori could be different between cancer and non-cancer patients. METHODS: H. pylori were isolated from gastric mucosal biopsy specimens obtained from 269 Koreans, who did not have any eradication therapy history and were diagnosed as one of the following diseases; chronic gastritis, benign gastric ulcer, duodenal ulcer or gastric cancer. The susceptibilities of the H. pylori isolates to amoxicillin, clarithromycin, metronidazole, tetracycline, azithromycin, ciprofloxacin, levofloxacin and moxifloxacin were examined with the agar dilution method. In addition, eradication rate of H. pylori was evaluated. RESULTS: There was no significant difference in the primary antibiotic resistance to above eight antibiotics among chronic gastritis, peptic ulcer disease and gastric cancer. Furthermore there was no difference of antibiotic resistance between cancer and non-cancer patients, and there was no difference of eradication rate of H. pylori according to disease. CONCLUSIONS: Primary antibiotic resistance and H. pylori eradication rate were not different between cancer and non-cancer patients.
2-Pyridinylmethylsulfinylbenzimidazoles/therapeutic use ; Adult ; Aged ; Amoxicillin/therapeutic use ; Anti-Bacterial Agents/therapeutic use ; Chronic Disease ; Clarithromycin/therapeutic use ; *Drug Resistance, Bacterial ; Drug Therapy, Combination ; Duodenal Ulcer/complications/microbiology ; Female ; Gastritis/complications/microbiology ; Helicobacter Infections/drug therapy/*epidemiology/microbiology ; Helicobacter pylori/*drug effects/isolation & purification ; Humans ; Male ; Microbial Sensitivity Tests ; Middle Aged ; Omeprazole/therapeutic use ; Peptic Ulcer/complications/microbiology ; Proton Pump Inhibitors/therapeutic use ; Republic of Korea ; Stomach Neoplasms/complications/microbiology

Emphysematous gastritis is a rare infection of the stomach wall with high mortality rate. It is caused by gas forming organisms and may arise by local spread through the mucosa or hematogenous dissemination from distant focus. Clinical manifestation includes acute abdomen with systemic toxicity, and diagnosis is based on radiologic demonstration of gas within the gastric wall. Treatment should be aimed to cover gram-negative organisms and anaerobes using wide-spectrum intravenous antibiotics, and sometimes surgical management may be needed in order to enhance survival. Herein, we report a case of emphysematous gastritis in a patient with end stage renal disease on hemodialysis.
Anti-Bacterial Agents/therapeutic use ; Emphysema ; Female ; Gastritis/complications/*diagnosis/radiography ; Gastroscopy ; Humans ; Kidney Failure, Chronic/complications/*diagnosis ; Klebsiella pneumoniae/isolation & purification ; Middle Aged ; Renal Dialysis ; Sputum/microbiology ; Tomography, X-Ray Computed

Gastric cancer is the second most common cause of cancer death worldwide and is usually detected at a late stage, except in Korea and Japan where early screening is in effect. Results from animal and epidemiological studies suggest that Helicobacter pylori infection, and subsequent gastritis, promote development of gastric cancer in the infected mucosa. Relatively effective treatment regimens are available to treat H. pylori infection, and in general, mass eradication of the organism is not currently recommended as a gastric cancer prevention strategy. However, regional guidelines vary regarding the indications and recommendations for H. pylori treatment for gastric cancer prevention. In this review, we discuss the results from intervention studies, provide insight regarding current guideline recommendations, and discuss future study directions.
Anti-Bacterial Agents/*therapeutic use ; Drug Therapy, Combination ; Early Detection of Cancer ; Evidence-Based Medicine ; Gastrectomy ; Gastritis/diagnosis/*drug therapy/microbiology ; Helicobacter Infections/complications/diagnosis/*drug therapy/microbiology ; Humans ; Neoplasm Recurrence, Local ; Practice Guidelines as Topic ; Proton Pump Inhibitors/*therapeutic use ; Risk Factors ; Stomach Neoplasms/diagnosis/microbiology/*prevention & control/surgery ; Treatment Outcome

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

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