Gastritis

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ESSENTIAL RESEARCH
Helicobacter pylori infection and the development of gastric cancer.
Gastric cancer develops in persons infected with H. pylori but not in uninfected persons. Those with histologic findings of severe gastric atrophy, corpus-predominant gastritis, or intestinal metaplasia are at increased risk. Persons with H. pylori infection and nonulcer dyspepsia, gastric ulcers, or gastric hyperplastic polyps are also at risk, but those with duodenal ulcers are not.
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ESSENTIAL RESEARCH
Helicobacter pylori infection induces gastric cancer in mongolian gerbils.
We have successfully demonstrated that long-term infection with H. pylori induces adenocarcinoma in Mongolian gerbils. The observations are thus highly suggestive of the involvement of H. pylori infection in gastric carcinogenesis in humans.
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ESSENTIAL RESEARCH
Helicobacter pylori and interleukin 1 genotyping: an opportunity to identify high-risk individuals for gastric carcinoma.
Combined bacterial/host genotyping may provide an important tool in defining disease risk and targeting H. pylori eradication to high-risk individuals.
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ESSENTIAL RESEARCH
Helicobacter pylori and atrophic gastritis: importance of the cagA status.
Infection with cagA-positive H. pylori strains is associated with an increased risk for the eventual development of atrophic gastritis and intestinal metaplasia.
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ESSENTIAL RESEARCH
Heightened inflammatory response and cytokine expression in vivo to cagA+ Helicobacter pylori strains.
These results indicate that infection with cagA+ H. pylori strains is associated with higher grades of gastric inflammation, correlating with enhanced mucosal levels of IL-8, and increased risk of peptic ulceration.
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ESSENTIAL RESEARCH
Campylobacter pylori antibodies in humans.
Campylobacter pylori infection, which is highly associated with active gastritis, may be diagnosed by serologic assay. Acquisition of infection begins in adult life, and prevalence increases with age.
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ESSENTIAL RESEARCH
Chemoprevention of gastric dysplasia: randomized trial of antioxidant supplements and anti-helicobacter pylori therapy.
In the very high-risk population studied, effective anti-H. pylori treatment and dietary supplementation with antioxidant micronutrients may interfere with the precancerous process, mostly by increasing the rate of regression of cancer precursor lesions, and may be an effective strategy to prevent gastric carcinoma.
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ESSENTIAL RESEARCH
Clinical relevance of Helicobacter pylori cagA and vacA gene polymorphisms.
We confirmed the associations of cagA and vacA polymorphisms with disease but now define their most important features. For cancer risk, among Western strains, the most important factor is the number of cagA EPIYA-C segment. For PU risk, it is the intermediate region type of vacA.
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Importance of Helicobacter pylori oipA in clinical presentation, gastric inflammation, and mucosal interleukin 8 production.
oipA functional status was related to clinical presentation, H. pylori density, and gastric inflammation. cag PAI, babA2, or vacA status appear important only as surrogate markers for a functional oipA gene.
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ESSENTIAL RESEARCH
A proinflammatory genetic profile increases the risk for chronic atrophic gastritis and gastric carcinoma.
These findings show that a proinflammatory polymorphism in the TNF-alpha gene is associated with increased risk for GC, and that it is possible to define a specific genetic profile associated with highest risk for CAG and GC.
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ESSENTIAL RESEARCH
Kyoto global consensus report on Helicobacter pylori gastritis.
A global consensus for gastritis was developed for the first time, which will be the basis for an international classification system and for further research on the subject.
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CD25+/Foxp3+ T cells regulate gastric inflammation and Helicobacter pylori colonization in vivo.
CD25+/Foxp3+ T cells actively participate in the immune response to H pylori. In vivo depletion of these cells in infected mice leads to increased gastric inflammation and reduced bacterial colonization.
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Atrophic gastritis and Helicobacter pylori infection in patients with reflux esophagitis treated with omeprazole or fundoplication.
Patients with reflux esophagitis and H. pylori infection who are treated with omeprazole are at increased risk of atrophic gastritis.
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Tolerance rather than immunity protects from Helicobacter pylori-induced gastric preneoplasia.
Using a novel CagA(+)H pylori infection model, we report here that the development of tolerance to H pylori protects from gastric cancer precursor lesions. The age at initial infection may thus account for the differential susceptibility of infected persons to H pylori-associated disease manifestations.
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Helicobacter pylori infection and chronic gastric acid hyposecretion.
In some subjects, chronic H. pylori infection produces a body-predominant gastritis and profound suppression of gastric acid secretion that is partially reversible with eradication therapy.
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Long term follow up of patients treated for Helicobacter pylori infection.
Preneoplastic gastric lesions regress at a rate equal to the square of time in patients rendered free of H pylori infection. Our findings suggest that patients with preneoplastic gastric lesions should be treated and cured of their H pylori infection.
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Mature chief cells are cryptic progenitors for metaplasia in the stomach.
These studies provide direct evidence by lineage tracing that SPEM evolves from differentiated chief cells. Thus, mature gastric chief cells have the ability to act as cryptic progenitors and reacquire proliferative capacity within the context of mucosal injury and inflammation.
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Induction of various cytokines and development of severe mucosal inflammation by cagA gene positive Helicobacter pylori strains.
These findings suggest that the ability to induce cytokines differs among the strains; cagA+ strains induce various kinds of cytokines and may cause severe inflammation, whereas cagA- strains induce IL-8 and IL-1 beta only weakly and may cause only mild inflammation. However, as most patients infected with the cagA+ strains have gastritis, these strains may not be equivalent to ulcerogenic strains.
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Lack of commensal flora in Helicobacter pylori-infected INS-GAS mice reduces gastritis and delays intraepithelial neoplasia.
Gastric lesions take 13 months longer to develop in germfree INS-GAS mice than male SPF INS-GAS mice. H pylori monoassociation accelerated gastritis and GIN but caused less severe gastric lesions and delayed onset of GIN compared with H pylori-infected INS-GAS mice with complex gastric microbiota. Changes in gastric microbiota composition might promote GIN in achlorhydric stomachs of SPF mice.
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A functional polymorphism of toll-like receptor 4 gene increases risk of gastric carcinoma and its precursors.
Our data suggest that the TLR4+896A>G polymorphism is a risk factor for noncardia gastric carcinoma and its precursors. The findings underscore the role of the host innate immune response in outcome of H pylori infection.
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ABOUT
Gastritis is inflammation of the lining of the stomach. It may occur as a short episode or may be of a long duration. There may be no symptoms but, when symptoms are present, the most common is upper abdominal pain. Other possible symptoms include nausea and vomiting, bloating, loss of appetite and heartburn. Complications may include bleeding, stomach ulcers, and stomach tumors. When due to autoimmune problems, low red blood cells due to not enough vitamin B12 may occur, a condition known as pernicious anemia.Wikipedia
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