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

In patients with diseases known to be associated with Helicobacter pylori infection, such as peptic ulcer, treatment of the underlying infection is the standard of care. However, in most major consensus management guidelines, including those published in Canada, widespread testing for H pylori infection is not recommended. This practice is not encouraged because of insufficient evidence of cost-benefit in gastric cancer prevention, the potential for increases in antibiotic resistance and the controversial hypothesis of potential negative effects of eradication in certain clinical entities. For example, there is insufficient evidence to recommend against eradicating H pylori discovered in a patient with symptoms of gastroesophageal reflux disease. The management guidelines designed specifically in Canada should, therefore, continue to be applied, with H pylori diagnosed and treated in appropriately selected patients.
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PMID:Risks and benefits of Helicobacter pylori eradication: current status. 1182 40

Helicobacter pylori infects half of the world's population, and is associated with asymptomatic gastritis and also with more serious conditions such as peptic ulcer disease and gastric carcinoma. The clinical outcome is largely dependent on the severity and distribution of the H pylori-induced gastritis, but the pathogenesis remains poorly understood. Bacterial virulence factors and environmental influences contribute to the pathogenesis, but do not explain the divergent outcomes. There is emerging evidence that host genetic factors play a key role in determining the clinical outcome of H pylori infection. In particular, proinflammatory genotypes of the interleukin-1 beta (IL-1b) gene are associated with an increased risk of gastric cancer and its precursors. The effects are most likely mediated through the induction of hypochlorhydria and severe corpus gastritis with the subsequent development of gastric atrophy. The roles of IL-1b and other host genetic factors in the pathogenesis of H pylori related cancer are discussed in this article.
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PMID:The role of interleukin-1beta and other potential genetic markers as indicators of gastric cancer risk. 1284 45

The relationship between Helicobacter pylori infection and the risk of gastric cancer has been well established in the last decade. Four meta-analyses have found that the infection increases the risk of noncardia gastric cancer by 2- to 6-fold compared with noninfected control populations. However, the role of cagA strains of H pylori in relation to gastric cancer has not been evaluated systematically. We undertook a meta-analysis of epidemiological studies examining the relationship between infection with cagA-positive strains of H pylori and the risk of gastric cancer, and found that patients who are seropositive for cagA strains of H pylori are at an increased risk for developing noncardia gastric cancer compared with those with H pylori infection alone. Therefore, searching for cagA-positive strains of H pylori may help identify populations at a greater risk for developing gastric cancer.
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PMID:The evolving epidemiology of Helicobacter pylori infection and gastric cancer. 1284 46

Medical ethics are not absolute; they change according to social attitudes, technological advances and alterations in the doctor/patient relationship. The discovery of Helicobacter pylori highlighted entrenched attitudes in academia and the pharmaceutical industry that were not always appropriate. The explosion of research that followed was ethically controlled by local research ethics committees and the system of peer review and editorial responsibility. Now that effective treatments are available, the control arm in trials of new therapy should be either placebo (giving the option of effective treatment later) or a first-line treatment; mono and dual therapy should not be employed because of the risk of inducing bacterial resistance. Ethical issues that still remain include whether always to test patients for H pylori at endoscopy and what information should be given when they test positive. The most important issue is the approach of the medical profession to the high death rate carried by H pylori infection. Peptic ulcer and gastric cancer together account for a large number of deaths worldwide, and the medical profession and public health services have not yet grappled with this problem, neither advocating universal testing and treatment nor funding or research to determine whether this approach would be effective.
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PMID:Ethical issues in the management of Helicobacter pylori infection. 1284 55

Helicobacter pylori infection is acquired in childhood, plays a causative role in chronic gastritis and peptic ulcer disease, and is associated with the development of gastric cancer. The present review focuses on recent advances in the scientific knowledge of H pylori infection in children, including clinical sequelae, diagnosis and treatment. In addition, recent insights regarding both bacterial and host factors that mediate human diseases associated with H pylori infection are discussed.
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PMID:Recent advances in Helicobacter pylori infection in children: from the petri dish to the playground. 1291 20

Experimental infection with Helicobacter pylori in Mongolian gerbils results in chronic gastritis and gastric cancer. To investigate epithelial cell proliferation, apoptosis, and mucosal cytokine responses in gastritis, Mongolian gerbils were infected with the H pylori SS1 strain. At 4 weeks post-infection, gastritis was predominantly within the antrum, but extended to the corpus in approximately 50% of gerbils by 36 weeks. Epithelial cell proliferation and apoptosis in glandular epithelial cells were increased with infection. Antral cell proliferation, but not apoptosis, correlated significantly with gastric inflammation. In female gerbils, H pylori significantly increased expression of transcripts for IFN-gamma and IL-12p40, but not TGF-beta or IL-10, in the gastric mucosa. Significantly reduced IFN-gamma and IL-12p40 responses were observed in male gerbils infected with H pylori, but epithelial proliferative and apoptotic responses were comparable to those of females. These studies demonstrate that the female gerbil cytokine response to H pylori has a Th1 profile and that there are gender differences in the magnitude of the gastric cytokine responses to H pylori. The absence of a down-regulatory cytokine response may account for the more severe gastritis observed with H pylori infection in gerbils than in mice.
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PMID:Gastric mucosal cytokine and epithelial cell responses to Helicobacter pylori infection in Mongolian gerbils. 1474 2

Helicobacter pylori up-regulates cyclo-oxygenase-2 (COX-2) expression, which in turn is involved in tumourigenesis. Recently, a causal link between COX-2 and multidrug resistance 1 (MDR-1) gene expression, implicated in cancer chemoresistance, has been demonstrated. Thus, the expression of COX-2 and the downstream enzyme involved in PGE2 biosynthesis, microsomal PGE-synthase1 (mPGES1), was correlated with P-gp, the product of MDR-1, and the anti-apoptotic protein, Bcl-xL, in gastric biopsies from patients with H pylori infection and in patients with gastric cancer. In a retrospective analysis of endoscopic and pathology files, 40 H pylori-negative patients (Hp-), 50 H pylori-positive patients who responded to eradication therapy (Hp+R), 84 H pylori-positive patients who did not respond to eradication therapy (Hp+NR), and 30 patients with gastric cancer (18 intestinal and 12 diffuse types) were selected. COX-2, mPGES1, P-gp, and Bcl-xL were detected by immunohistochemistry. COX-2, mPGES1, P-gp, and Bcl-xL expression was undetectable in gastric mucosa from Hp- patients. By contrast, COX-2 and mPGES1 expression was detected in 42% and 44% of Hp+R patients, respectively, and in up to 66% (range 63-66%) of Hp+NR patients (p < 0.05). The expression of COX-2 and mPGES1 correlated significantly (p < 0.0001) with that of P-gp and Bcl-xL. High levels of COX-2, mPGES1, P-gp, and Bcl-xL expression were found in intestinal-type gastric cancer samples. In conclusion, H pylori-dependent induction of COX-2 and mPGES1 is associated with enhanced production of P-gp and Bcl-xL that may contribute to gastric tumourigenesis and resistance to therapy.
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PMID:Expression of COX-2, mPGE-synthase1, MDR-1 (P-gp), and Bcl-xL: a molecular pathway of H pylori-related gastric carcinogenesis. 1499 95

As an update to previously published recommendations for the management of Helicobacter pylori infection, an evidence-based appraisal of six topics was undertaken in a consensus conference sponsored by the Canadian Helicobacter Study Group. The issues addressed and recommendations made were: bismuth-containing quadruple therapy is appropriate as an alternative first-line eradication strategy for H pylori infection; searching for and treating H pylori infection is warranted in patients considered to be at high risk for gastric cancer; H pylori infection should be eradicated before initiating long-term treatment with nonsteroidal anti-inflammatory drugs or acetylsalicylic acid; the stool antigen test has a limited role in the diagnosis of H pylori infection; the benefits of H pylori eradication in patients on long-term proton pump inhibitor therapy are not sufficient to warrant recommending a strategy of searching for and eradicating the infection among these patients; and a strategy of "test and eradicate" for H pylori infection in patients with uninvestigated dyspepsia is cost-effective in Canada relative to a trial of proton pump inhibitor therapy. The goal was to establish guidelines on the best evidence using the same structure to address and formulate recommendations for each issue. The degree of consensus for each issue is presented.
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PMID:Canadian Helicobacter Study Group Consensus Conference: Update on the management of Helicobacter pylori--an evidence-based evaluation of six topics relevant to clinical outcomes in patients evaluated for H pylori infection. 1545 93

Helicobacter pylori infection is acquired primarily during childhood and carries a significant lifetime risk for morbidity. In developing countries, approximately 70% of children are infected with the bacterium by their 15th birthday. In the United States, the rate of H pylori infection among children varies widely--approximately 10% of all 10-year-olds are infected; however, this figure is substantially higher among populations of immigrant children and children born of recent immigrants to the United States. H pylori transmission is primarily "person-to-person" via fecal-oral, gastric-oral, or oral-oral routes, with evidence suggesting contaminated water as a potential source of infection. Risk factors for infection in childhood include an infected family member, having > or =2 siblings, crowded living conditions, lower socioeconomic means, and attendance at a daycare facility. The natural history of H pylori infection includes an increased lifetime risk for peptic ulcer and gastric adenocarcinoma or lymphoma. In children and adults who develop H pylori-related peptic ulcer, cure of the infection is associated with a <5% rate of ulcer recurrence. The ideal mode of H pylori detection among children is unclear--currently available serology and whole blood tests are unreliable, while the urea breath test and stool antigen tests have not been studied adequately. Children with confirmed H pylori-related peptic ulcer disease, iron-deficiency (sideropenic) anemia, or a first-degree relative with gastric cancer should be treated for the infection using 1 of 3 available 10- to 14-day triple therapy regimens recommended by the North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition.
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PMID:Appropriate strategies for testing and treating Helicobacter pylori in children: when and how? 1547 50

Gastric adenocarcinoma is a disease of high mortality and poor prognosis that is second only to lung cancer as a leading cause of cancer-related deaths worldwide. Although gastric cancer has a multifactorial etiology, infection with Helicobacter pylori is highly associated with its development. New information on bacterial and host genetics and results of epidemiologic studies suggest that better identification of individuals at high risk for gastric malignancy may be possible. Studies suggest that cure of H pylori infection may be associated with retardation of glandular atrophy and intestinal metaplasia but not reversal of dysplasia. Theoretically, it is attractive to believe that eradication of H pylori infection might prevent gastric cancer; however, studies supporting this hypothesis are not yet available. Public policy strategies for the identification of patients at risk for H pylori-related gastric malignancy are likely to be complex, but testing and treating for the infection earlier rather than later in life is anticipated to be the more beneficial approach.
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PMID:Will eradication of Helicobacter pylori infection influence the risk of gastric cancer? 1547 58


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