Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Helicobacter pylori (H. pylori) infection is associated with peptic ulcer disease and gastric cancer. The eradication of H. pylori is of special interest in patients with congenital bleeding disorders, for whom treatment of gastrointestinal hemorrhage with factor concentrates is costly. The prevalence of H. pylori varies between different populations and identification of high-risk subgroups may allow for more targeted screening and eradication of the infection. We performed a 5-year retrospective study of gastrointestinal bleeding, combined with screening and treatment for H. pylori and a long-term prospective follow-up in 168 Swedish and 23 Estonian patients with hemophilia or von Willebrand disease. The prevalence of seropositivity was lower in Sweden than in Estonia (28 versus 48%, p = 0.03), lower in native Swedes than in non-Nordic immigrants to Sweden (20 versus 76%, p = 0.0001) and lower in patients less than 40 years of age than older patients (16 versus 38%, p = 0.002). The incidence of gastrointestinal hemorrhages among the 35 Swedish patients with active H. pylori infection, confirmed by a urea breath test, was 6.0 per 100 patient-years before eradication therapy versus 1.7 during the prospective followup. A negative urea breath test one month after therapy always remained negative after one year. Screening, followed by treatment of all infected patients, yielded a reduction of direct costs over a 5-year period of 130 US-$ per screened patient. We conclude that screening and eradication therapy for infection with H. pylori in patients with congenital bleeding disorders is an effective and economic strategy.
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PMID:Helicobacter pylori causes gastrointestinal hemorrhage in patients with congenital bleeding disorders. 1266 30

Helicobacter pylori (H. pylori) eradication treatment should always be thought of as a package which includes first and second line therapies together. So, testing of H. pylori eradication following first line treatment should always be performed and should be explained to the patient with the prescription of the triple therapy. For confirmation of H. pylori eradication both the urea breath test and the biopsy based test (when endoscopy is clinically indicated) are recommended. Stool antigen test is also an accurate test although it seems to have a lower diagnostic value after eradication treatment. Testing should be performed at least of 4 weeks after treatment. Serology with pre and 6 months post treatment samples is usually not recommended except in the case of H. pylori eradication campaign in populations at high risk for stomach cancer for instance.
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PMID:[Confirmation of Helicobacter pylori eradication following first line treatment. How and when?]. 1270 May 5

Helicobacter pylori chronically infects half of the human population and is associated with gastritis, peptic ulcer and gastric cancer. (13)C-urea breath test (UBT) is the main in vivo tool for the diagnosis of H. pylori infection. In this study, the safety and the accuracy of UBT were evaluated. A group of 492 dyspeptic patients was studied by UBT, the results were expressed as the difference over baseline at 30 min (DOB30). All patients were evaluated for systemic, gastrointestinal or allergic-type adverse reactions after ingestion of 75 mg (13)C-urea and citric acid in aqueous solution. The first 256 patients enrolled also underwent endoscopy and gastric biopsy. Patients positive on histology were considered infected. UBT was well tolerated and none of the 492 patients had any systemic or allergic-type adverse reaction. Among the 256 patients studied with histology, 116 were H. pylori positive on biopsies. Using 4 %o as cut-off value for DOB30,115 out of the 256 patients were positive on UBT, with only 2 false positive and 3 false negative. With this threshold, the sensitivity, specificity, and accuracy of the UBT were 97.4%, 98.5%, and 98.0%, respectively. (13)C-UBT has proven to be a safe and simple, yet accurate, test for the non-invasive diagnosis and monitoring of H. pylori infection.
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PMID:Usefulness of (13)C-urea breath test in the diagnosis of gastric helicobacter pylori infection. 1274 75

H. pylori infection of the gastric mucosa is associated with increased epithelial cell apoptosis. In vitro, interferon-gamma and TNF-alpha have been shown to increase the sensitivity of cells to apoptosis induced by H. pylori. The p53 tumor suppressor gene is frequently mutated in many cancers, including gastric cancer. Since p53 protein can induce apoptosis, we sought to determine whether or not p53 increases the ability of gastric epithelial cells to undergo apoptosis in response to H. pylori-induced cell injury. Human gastric epithelial cell lines, AGS (p53 wild-type) cells and AGS cells infected with HPV E6 gene (AGS-E6) to inactivate p53 were exposed to H. pylori. The p53, p21, and p14ARF proteins were measured in gastric epithelial cells by immunoelectrophoresis. Gastric epithelial cell apoptosis was measured by DNA end-labeling assay (TUNEL) and subG0 cell fractions using flow cytometry, and by agarose gel electrophoresis of DNA. Exposure to H. pylori increased the levels of p53, p21, and p14ARF proteins two fold in AGS cells. Gastric AGS cells with fragmented DNA increased from 1.1% to 68% in after exposure to H. pylori for 24 hr. However, AGS-E6 cells were relatively resistant to apoptosis induced by H. pylori (only 15% of cells underwent apoptosis). In additional experiments, mouse embryonic fibroblasts (MEFs) were used to further investigate the role of ARF in stabilizing p53 after exposure to H. pylori. Wild-type and p19ARF-/- MEFs were exposed to H. pylori and evaluated for activation of p53, p19ARF, and apoptosis. As with AGS cells, H. pylori stimulated a 2-fold increase in p53 and p19ARF in wild-type MEFs; however, there was no increase in p53 in ARF-null MEFs. H. pylori easily stimulated apoptosis in wild-type MEFs, although, the absence of p19ARF significantly reduced the ability of H. pylori to induce apoptosis in these cells. Activation of ARF by H. pylori is important in stabilizing p53 resulting in increased apoptosis. Thus, inactivation of either ARF or p53 in gastric cells may reduce their ability to undergo apoptosis in response to injury induced by H. pylori.
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PMID:p53 and p14 increase sensitivity of gastric cells to H. pylori-induced apoptosis. 1287 Jul 84

Helicobacter pylori (H. pylori) is a spiral shaped bacterium that resides in the stomach mucosa. Isolation of H. pylori from the stomach mucosa changed the erstwhile widely held belief that the stomach contains no bacteria and is actually sterile. Once H. pylori is safely ensconced in the mucus, it is able to neutralize the acid in the stomach by elaborating an enzyme called urease. Urease converts urea, of which there is an abundant supply in the stomach (derived from saliva and the gastric juice), into bicarbonate and ammonia, which are strong bases. These bases form a cloud of acid-neutralizing chemicals in the vicinity of the organisms, protecting them from the acid in the stomach. This urea hydrolysis reaction is utilized for the diagnosis of H. pylori infection in the urea breath test (UBT) and the rapid urease test (RUT). In Japan, both invasive tests, such as bacterial culture, histopathology and RUT, and non-invasive tests such as UBT and serology are conducted for the diagnosis of H. pylori infection. For confirming the results of eradication therapy, UBT is considered to be the most sensitive and specific. In order to treat H. pylori infection, a new one-week triple therapy regimen (lansoprazole or omeprazole + amoxicillin + clarithromycin) has been approved for use in patients with peptic ulcer disease in Japan. As for H. pylori eradication in the case of other diseases in which the bacterium has been implicated (e.g., chronic atrophic gastritis, gastric MALT lymphoma, gastric cancer, non-ulcer dyspepsia, chronic urticaria, idiopathic thrombocytopenic purpura (ITP)), further basic and clinical investigation is required.
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PMID:Current consensus on the diagnosis and treatment of H. pylori-associated gastroduodenal disease. 1452 49

Helicobacter pylori infects approximately half the human population. The outcomes of the infection range from gastritis to gastric cancer and appear to be associated with the immunity to H. pylori. Patients developing nonatrophic gastritis present a Th1 response without developing protective immunity, suggesting that this bacterium may have mechanisms to evade the immune response of the host. Several H. pylori proteins can impair macrophage and T cell function in vitro through mechanisms that are poorly understood. We tested the effect of H. pylori extracts and live H. pylori on Jurkat cells and freshly isolated human normal T lymphocytes to identify possible mechanisms by which the bacteria might impair T cell function. Jurkat cells or activated T lymphocytes cultured with an H. pylori sonicate had a reduced proliferation that was not caused by T cell apoptosis or impairment in the early T cell signaling events. Instead, both the H. pylori sonicate and live H. pylori induced a decreased expression of the CD3zeta-chain of the TCR. Coculture of live H. pylori with T cells demonstrated that the wild-type strain, but not the arginase mutant rocF(-), depleted L-arginine and caused a decrease in CD3zeta expression. Furthermore, arginase inhibitors reversed these events. These results suggest that H. pylori arginase is not only important for urea production, but may also impair T cell function during infection.
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PMID:Helicobacter pylori arginase inhibits T cell proliferation and reduces the expression of the TCR zeta-chain (CD3zeta). 1521 Aug 20

Endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) has become a fundamental procedure for gastrointestinal and lung cancer staging. However, there is growing evidence that micrometastases are present in lymph nodes, which cannot be detected with standard pathological methods. The aim of this study was to evaluate whether hypermethylation gene promoter analysis was feasible on samples obtained by EUS-FNA from lymph nodes, as well as to establish the usefulness of this strategy for the detection of micrometastases in patients with gastrointestinal and non-small cell lung cancer. Suspicious lymph nodes based on EUS findings from consecutive patients with esophageal, gastric, rectal, and non-small cell lung cancer were sampled by EUS-FNA. Hypermethylation analysis of the MGMT, p16(INK4a), and p14(ARF) gene promoter CpG islands were performed by methylation-specific PCR. Effectiveness of conventional cytology, methylation analysis, and their combination were established with respect to the definitive diagnosis. Twenty-seven patients were included, thus representing a total of 42 lymph nodes (esophageal cancer, n = 11; rectal cancer, n = 7; gastric cancer, n = 3; and lung cancer, n = 21). According to definitive diagnosis, 21 (50%) corresponded to metastatic lymph nodes. Sensitivity, specificity, and overall accuracy of conventional cytology were 76%, 100%, and 88%, respectively, whereas the corresponding values for the methylation analysis were 81%, 67%, and 74%, respectively. Combination of both techniques increased sensitivity (90%) but decreased specificity (67%) with respect to conventional cytology. In conclusion, it is feasible to detect occult neoplastic cells in EUS-FNA samples by hypermethylation gene promoter analysis. Moreover, addition of methylation analysis to conventional cytology may increase its sensitivity at the expenses of a decrease in its specificity.
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PMID:Detection of lymph node micrometastases by gene promoter hypermethylation in samples obtained by endosonography- guided fine-needle aspiration biopsy. 1524 May 35

The importance of atrophic gastritis with intestinal metaplasia is related to the fact that it increases the risk of gastric cancer development. The aim of this study is to evaluate the diagnostic potential of serum pepsinogens in predicting the topography of intestinal metaplasia. Both dye endoscopy and 13C-urea breath test were carried out in 878 subjects. Serum pepsinogen I, pepsinogen II, and IgG antibody to Helicobacter pylori were measured. The overall prevalence of intestinal metaplasia was higher in subjects with lower PG I/II ratios and lower PG I values. Based on ROC curves, a cutoff value for pepsinogen I/II ratio of less than 3.0 would have identified intestinal metaplasia with a sensitivity of 71.7% and a specificity of 66.7% in Helicobacter pylori-positive subjects. It is possible that serum pepsinogens could be used as a screening test for high-risk subjects with intestinal metaplasia.
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PMID:Serum pepsinogens as a predicator of the topography of intestinal metaplasia in patients with atrophic gastritis. 1525 1

The proposed route of Helicobacter pylori transmission appears to be fecal-oral, oral-oral and gastro-oral, yet, a number of studies challenged these hypotheses in 2003. The use of the stool antigen test and[13]-C urea breath testing were the tests of choice for diagnosis and 'test for cure' of H. pylori in Europe in 2003 but have not yet become accepted standard of care in North America. Pediatric H. pylori consensus guidelines are not yet revised; upper endoscopy and biopsy remain the gold standard for diagnosis of pediatric H. pylori infection. In addition to stronger evidence supporting the role of host influences of H. pylori-associated gastric cancer risk, compelling evidence was provided for the role of H. pylori in iron deficiency anemia of childhood. Antibiotic resistance remains a problem in conferring treatment failure and 2003 studies indicate that macrolide resistance is higher in children than in adults. Treatment with proton pump inhibitor-based triple therapy for 10-14 days remains the mainstay for eradication of H. pylori in childhood. Finally, multinational studies are needed to develop screening guidelines for childhood infection to avoid long-term severe gastroduodenal disease sequelae.
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PMID:Helicobacter pylori infection in pediatrics. 1534 6

The longitudinal stability of the urea breath test (UBT), which measures urease as a biomarker for infection with Helicobacter pylori (a major risk factor for gastric cancer), was evaluated in the environs of Tsukuba, Japan. 13C-UBT measurements were monitored at four time points in 46 free-living, H. pylori-infected, asymptomatic volunteers over a period of 7 weeks. Subjects were asked to refrain from eating cruciferous vegetables, which might confound interpretation of results. Their compliance was monitored using both dietary records and direct biochemical testing of overnight urine. There was large between-subject UBT variation in this population (logUBT mean, 3.34; SD, 0.67). Within-subject (longitudinal) UBT values were remarkably stable in about one-quarter of the subjects (coefficients of variations for these individuals were <21%), whereas coefficients of variations in the highest quartile of variability ranged from 40% to 80%. About half of the sequential UBTs (63 of 138 such measurement pairs) changed >10 per thousand "delta over baseline" between measurements. This study provides the elements to optimize the design of a clinical trial in this population to examine the efficacy of a dietary intervention to reduce H. pylori infection. The number of subjects required to detect a 30% difference in average UBT value is highly dependent on the baseline stability of UBT measurements. For the least variable quartile, as few as 12 subjects would be needed; for the most variable quartile, at least 147 subjects would be required in each arm.
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PMID:Dietary amelioration of Helicobacter pylori infection: design criteria for a clinical trial. 1546 77


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