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

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

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

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: 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

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

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

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