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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

H. pylori infection is strongly implicated in the pathogenesis of peptic ulcer disease and gastric cancer. Although the infection may be detected in over half the world's population, only a proportion will develop either ulcer disease or gastric cancer. The prevalence of the infection is very high in both diseases, but other factors combined with chronic infection must lead to specific clinical manifestations of the disease. Long-standing infection results in chronic active gastritis. In a certain subset of the H. pylori-infected population, factors such as dietary, environmental, and/or genetic factors, or specific strains of the bacterium, may result in the expression of one disease or another. There are now many investigations into these various aspects of association of the infection and disease outcome which may lead to elucidation of the actual processes in the development of specific disease in the H. pylori-infected patient. Many different tests are now available for accurate diagnosis of the infection. The non-invasive tests include the serologic tests, which include both the ELISA and the rapid-immunoassay, and the urea breath test. Invasive tests can be performed on the patient at the time of endoscopy when tissue specimens can be taken for the rapid urease test, histology, or culture.
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PMID:Helicobacter pylori: its role in ulcer disease and gastric cancer and how to detect the infection. 913 57

Infection with Helicobacter pylori (H. pylori) plays an important role in the pathogenesis of gastritis, peptic ulcer and gastric cancer, and the 13C-urea breath test (13C-UBT) is a convenient and non-invasive method for the detection of H. pylori in the stomach. We have examined the sensitivity, specificity and accuracy of 13C-UBT. The 13CO2/12CO2 ratio was measured using infrared spectroscopy (IR) and gas chromatography/mass spectrometry (GC-MS).
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PMID:Validity of the 13-C-urea breath test for the diagnosis of Helicobacter pylori infection. 914 10

Indications for eradication of Helicobacter pylori infection have widened since the National Institutes of Health consensus conference in 1994. It is argued that they should now include infected patients with non-ulcer dyspepsia, those concerned about the risk of gastric cancer, patients with gastric lymphoma, and those requiring long-term treatment with a proton pump inhibitor. Problems with existing clinical trials are discussed, and the results of different treatment regimens are discussed. It is proposed that future eradication trials should investigate H. pylori-infected subjects identified by serology, rather than ulcer patients, and that eradication is proved only by a pair of 13C-urea breath tests.
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PMID:The treatment of Helicobacter pylori infection. 914 89

Helicobacter pylori is associated with primary antral gastritis, duodenal ulceration, and gastric cancer. Current regimens for treating infection in children using bismuth and antibiotics for two to six weeks are cumbersome. The aim of this study was to evaluate a one week course of treatment. All children undergoing endoscopy were assessed for the presence of H pylori by culture, histology, rapid urease test, and 13C urea breath test. Infected children received a one week course of colloidal bismuth subcitrate 480 mg/1.73 m2/day (maximum 120 mg four times a day), combined with metronidazole 20 mg/kg/day (maximum 200 mg three times a day), and clarithromycin 15 mg/kg/day (maximum 250 mg twice a day). To optimise compliance, drugs were dispensed in a 'Redidose' box containing a compartment for each day, and subcompartments marked 'breakfast', 'lunch', 'dinner', and 'bedtime'. Compliance and side effects were assessed immediately after treatment. A urea breath test was performed at least one month after treatment. Twenty two children infected with H pylori were entered into the study; 20 of these took all doses; two children suffered significant side effects (diarrhoea and vomiting). H pylori was eradicated in 21 of the 22 children (95.45%; 95% confidence interval 77% to 100%). This study shows that H pylori infection in children can be cleared by a one week course of treatment.
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PMID:One week treatment for Helicobacter pylori infection. 916 31

Helicobacter pylori has been established as the major causative agent of human active gastritis and is an essential factor in peptic ulcer disease and gastric cancer. The mechanism that has been proposed for H. pylori to control its inhospitable microenvironment happens to coincide with the pH control technique developed by us. This technique was developed to separate an acidic environment from a basic environment for a sequential enzymatic reaction by the hydrolysis of urea within a thin layer of immobilized urease. In this paper, a mathematical model is presented to consider how H. pylori survives the gastric acidity. The computed results explain well the experimental data available involving H. pylori.
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PMID:Helicobacter pylori survival in gastric mucosa by generation of a pH gradient. 925 24

The ideal approach for the initial diagnosis of Helicobacter pylori infection is to perform an endoscopy to obtain biopsy specimens for histology and culture. Histology allows classification of any gastritis lesions present and may have prognostic value, and culture enables susceptibility testing of antimicrobial agents to direct proper treatment. Biopsy specimens must also be taken from the corpus if the patient was pretreated with proton pump inhibitors. The cost of these tests and the delay in receiving results limits their use in clinical practice. Therefore, the urease test, a quick and inexpensive test, is used to detect the presence of H. pylori and constitutes the basic invasive test for H. pylori. A new urease test based on a strip instead of an agar disk may be the test of choice in the future, because of its increased sensitivity and 2-hour delay (instead of 24 hours) in obtaining the result. In some countries, because of the cost, endoscopy will be used in selected patients only, either because of alarm symptoms or age > 45 years, which is considered a threshold for gastric cancer risk. In other patients, the noninvasive tests will be used. The cost of serology makes it more attractive compared with the urea breath test. Currently, there are accurate enzyme-linked immunosorbent assay tests that can be performed in any laboratory and that provide precise and quick diagnoses. In the event of a doubtful result, an immunoblot can be performed, as is the case for other infections. Patient follow-up after treatment provides a different situation because bacterial load is usually lower. A noninvasive test should be performed, and only the urea breath test can be used within the timing originally proposed to test eradication efficacy (i.e., 4-6 weeks after treatment). If the result is positive, susceptibility testing is required before administering a second course of treatment. The increasing use of antimicrobial agents to treat H. pylori is likely to result in antimicrobial resistance, requiring that bacteriologic surveillance programs be implemented. There are numerous research projects ongoing in this area, and one can expect that improved methods, such as colorimetric polymerase chain reaction (PCR) and improved antibody tests, will also be used in the future.
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PMID:How should Helicobacter pylori infection be diagnosed? 939 68

Several areas regarding Helicobacter pylori that need improvement or clarification in the United States include treatment of dyspepsia, physician education on disease associations with H. pylori, and evidence from U.S. studies that 7-day H. pylori eradication regimens are more effective than current regimens. Dyspepsia, a ubiquitous condition in the United States, is routinely managed on the basis of a positive H. pylori serology without other investigations. This approach has been fostered by cost-effectiveness studies of various approaches to duodenal ulcer and dyspeptic patients. Serology-directed therapy was the most cost-effective option vs. endoscopy-directed management. The option of not obtaining endoscopy had broad appeal to primary care physicians. In addition, a recent survey suggests that even gastroenterologists routinely attempt H. pylori eradication in infected patients with nonulcer dyspepsia, despite a number of negative efficacy studies. Finally, the option of not eradicating a World Health Organization-defined carcinogen in the litigious United States is unappealing to clinicians. Eradication of H. pylori in patients with dyspepsia despite more negative trials is likely to continue. There is evidence that U.S. physician awareness of the H. pylori-disease associations and the best therapies are improving rapidly, but further improvement is needed. Discrepancy of awareness of H. pylori between gastroenterologists and family physicians exists. In a recent survey, 94% and 72% of gastroenterologists regarded H. pylori as a causative agent in duodenal and gastric ulcer, respectively, vs. 68% and 68% of family physicians, and only 9% of family physicians believed there was a definite relationship between H. pylori infection and gastric cancer vs. 21% of gastroenterologists. One hundred three different H. pylori regimens were being used; 31% of family physicians and 11% of gastroenterologists used ineffective regimens or regimens of unknown effectiveness. Although 1-week proton pump inhibitor triple therapy is promising, there is skepticism that U.S. studies will yield the optimistic results that have characterized the European studies. Unlike in Europe, the U.S. standard is to use double diagnostics to prove eradication rather than just the urea breath test and to use intent-to-treat rather than assessable patient analyses. Both approaches reduce apparent eradication rates.
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PMID:What remaining questions regarding Helicobacter pylori and associated diseases should be addressed by future research? View from North America. 939 80

Many putative virulence determinants of Helicobacter pylori are believed to trigger and worsen the gastroduodenal mucosa damage observed in infected patients. H. pylori urease reacts with the gastric urea and generates ammonia; ammonia combines with water and yields ammonium hydroxide, which is cytotoxic. Ammonia may also inhibit cell proliferation and cause indirect mucosal injury by stimulating neutrophils. Phospholipases may damage the gastric mucosa by degrading phospholipids and generating precursors of ulcerogenic components. Other enzymes, such as protease, neuraminidase, fucosidase, and alcohol dehydrogenase, can contribute to damage of the gastric epithelium by destroying the integrity of mucus or by inducing lipid peroxidation. Infection by vacuolating cytotoxic (VacA+) H. pylori strains is considered to constitute increased risk for development of peptic ulcer and gastric cancer. Exploration of the vacA gene structure has shown the existence of strongly toxigenic strains, and has confirmed at the molecular level the increased ulcerogenic potential of VacA+ H. pylori strains. A pathogenicity island called cag has been recently described in Type 1 H. pylori strains (VacA+/CagA+).cag contains the cagA gene (whose expression is associated with toxigenicity) and many genes, some of which are highly homologous to virulence genes of other virulent bacteria, that account for the enhanced pathogenic potential of CagA+ organisms.
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PMID:Helicobacter pylori factors involved in the development of gastroduodenal mucosal damage and ulceration. 947 42

Helicobacter pylori appears to play a major role in the development of gastric cancer in humans. The mechanism behind the carcinogenic or co-carcinogenic effects of H. pylori has not been established. Ammonia, generated by urea from H. pylori, has been studied as a possible cause. However, the ammonia-monochloramine system has been shown to play a more important role in H. pylori-associated mucosal injury. Therefore, the effects of combined administration of monochloramine and methionine, singly or together, on the development of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were investigated in inbred Wistar rats. After receiving oral MNNG and regular chow pellet for 25 weeks, rats received regular chow pellets or chow pellets containing 20% ammonium acetate, and normal tap water or water containing 30 mM sodium hypochlorite, with or without a subcutaneous injection of methionine, until the end of the experiment (week 52). Treatment with both ammonium acetate and sodium hypochlorite, which produce monochloramine, significantly increased the incidence of gastric cancers in week 52, whereas the concomitant administration of methionine with ammonium acetate and sodium hypochlorite significantly attenuated such enhanced gastric carcinogenesis. Spectrophotometric examination revealed that methionine scavenged monochloramine. Our findings suggest that H. pylori-associated gastric carcinogenesis may be mediated by monochloramine.
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PMID:Attenuation by methionine of monochloramine-enhanced gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats. 953 64

Helicobacter pylori, one of the most prevalent human pathogens, is associated with chronic gastritis, peptic ulcer disease, and possibly gastric cancer and primary gastric lymphoma. The need to treat these patients has necessitated the development of improved methods to diagnose H. pylori infection. We present the preliminary assessment of a 13C-urea breath test (UBT) in which the expired 13CO2 is detected in a rapid, simple, inexpensive way by the LARA (Laser Assisted Ratio Analyzer) System (Alimenterics, Inc., Morris Plains, NJ). Eighty-seven consecutive patients, examined for upper gastrointestinal symptoms, underwent endoscopy. H. pylori infection was established by antral biopsies and a rapid urease test (CLOtest). The UBT was performed between 2 and 24 hours after endoscopy. Of the 84 analyzable patients, 70 were found to be H. pylori-positive either by histology or by CLOtest. All 70 were positive by the LARA UBT, yielding a sensitivity of 100%. Fourteen patients were negative for H. pylori by histology and the CLOtest. Of these, 12 were negative by the LARA UBT and 2 were positive, yielding a specificity of 85.7%; because of the limitations of H. pylori detection by histology or urease assays, however, the specificity of the UBT may have been underestimated. Our study demonstrates the feasibility of a nonradioactive, rapid UBT based on the LARA system and suggests the need for its more detailed evaluation.
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PMID:A simplified urea breath test for the diagnosis of Helicobacter pylori infection using the LARA System. Laser Assisted Ratio Analyzer. 964 7


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