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

Infection of the stomach and the duodenum by Helicobacter pylori is the major cause of acute and chronic gastroduodenal pathologies in humans and increases the risk of gastric cancer. The recognition of the infectious nature of the illness is having a major impact in the management of the disease that is shifting from the treatment of symptoms by anti-H2 blockers to the eradication of the bacterial infection by antibiotic regimen. Experience with other bacterial diseases, suggests that antibiotic treatment will select resistant strains that in the long term will make the antibiotics infective. Vaccination that classically is the most effective way to prevent and control infectious diseases in large population, could be used to prevent infection and possibly also to treat the disease. Here we summarize the studies on the identification and characterization of the virulence factors that are important for the pathogenesis of the bacterium and that may be candidate components for a vaccine. Animal models of the infection are also described.
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PMID:Pathogenesis of Helicobacter pylori and perspectives of vaccine development against an emerging pathogen. 775 8

The human pathogen Helicobacter pylori is associated with gastritis, peptic ulcer disease, and gastric cancer. The pathogenesis of H. pylori infection in vivo was studied by adapting fresh clinical isolates of bacteria to colonize the stomachs of mice. A gastric pathology resembling human disease was observed in infections with cytotoxin-producing strains but not with noncytotoxic strains. Oral immunization with purified H. pylori antigens protected mice from bacterial infection. This mouse model will allow the development of therapeutic agents and vaccines against H. pylori infection in humans.
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PMID:Development of a mouse model of Helicobacter pylori infection that mimics human disease. 788 48

Helicobacter pylori is uniquely adapted to survival in the strongly acidic gastric lumen. In vitro, both acid and certain acid suppressors affect bacterial growth. In vivo, there is little evidence that acid suppressors have any effect on bacterial survival. In contrast, decrease of acid secretion quickly leads to a spreading of the bacterial infection throughout the body and fundus of the stomach, which is accompanied by an increase of the associated gastritis. Helicobacter pylori gastritis may, in a substantial number of infected subjects, ultimately lead to atrophy and intestinal metaplasia, conditions with an increased risk for gastric cancer. This review summarizes the data on the interrelation between Helicobacter pylori, gastric acid secretion and development of atrophic gastritis.
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PMID:Review article: the development of atrophic gastritis--Helicobacter pylori and the effects of acid suppressive therapy. 852 9

Gastric atrophy and intestinal metaplasia are considered the earliest phenotypic changes in the cascade of events leading from normal mucosa to intestinal-type gastric cancer, and epidemiological evidence links Helicobacter pylori to gastric epithelial malignancies. To evaluate any causal relationship between bacterial infection and atrophic metaplastic lesions, gastric pathology was histologically and histochemically evaluated in 267 consecutive, nonulcerous, untreated subjects, with attention given the phenotypes of intestinal metaplasia. The prevalence of Helicobacter pylori infection was 61%. Intestinal metaplasia (particularly types II and III) was significantly associated with both Helicobacter pylori detection (chi 2 LR: P < 0.002) and increasing age (chi 2 LR: P < 0.002). Using logistic regression analysis, the development of intestinal metaplasia proved more significantly linked with Helicobacter pylori infection [odds ratio = 4.55 (95% confidence interval: 1.51-13.7)], than with age [odds ratio = 1.03 (95% CI: 1.01-1.06)], with no interaction. In conclusion, Helicobacter pylori can be considered among the major causal agents of mucosal lesions involved in the multistep process of gastric carcinogenesis, justifying any attempt to eradicate this bacterial infection.
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PMID:Helicobacter pylori in promotion of gastric carcinogenesis. 862 68

Helicobacter pylori is probably the commonest bacterial infection worldwide and is now accepted as the cause of chronic active type B gastritis. Most patients continue through life with a chronic superficial gastritis while some develop either duodenal or gastric ulcer. In a very small proportion the lymphoid reaction to H. pylori infection appears to progress to become a mucosal associated lymphoid tissue (MALT) lymphoma, while in others the evidence suggests that chronic superficial gastritis progresses to atrophy, the loss of gastric acid secretory capacity and the development of gastric cancer. The mechanisms involving H. pylori infection in peptic ulceration are increasingly well understood and H. pylori is now accepted as having a critical role in duodenal ulcer, where the prevalence of infection is 90 to 95%. More important is the dramatic reduction in duodenal ulcer recurrence after successful eradication of the organism to about 4% in a year compared to recurrences of up to 80% in those who ulcers have been healed but in whom the infection persists. There is also increasing evidence for the involvement of H. pylori in gastric ulcer, where infection is seen in between 60 and 80%, and there is a similar dramatic reduction in recurrence following cure of H. pylori infection. The progression of H. pylori gastritis from the acute infection to chronic superficial gastritis, predominantly antral gastritis or a pangastritis with increasing atrophy appears to be associated with the differing outcomes seen in this disease. Moreover, there is increasing data on the roles played by bacterial heterogeneity and the virulence of the organism, host factors such as the HLA genotype and immune response, environmental factors and the age of acquisition of infection play in determining these clinical outcomes of the disease.
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PMID:The role of Helicobacter pylori in pathogenesis: the spectrum of clinical outcomes. 889 29

The colonization of gastric mucosa by Helicobacter pylori (H.p.) is a special form of chronic bacterial infection characterized by long term persistence of microbes because cause of an inefficiency of local immune responses. The resulting chronic gastritis causes decisive transformations of gastric mucosa. They comprise the acquisition of an active mucosa-associated lymphoid tissue as well as the development of glandular atrophy and intestinal metaplasia in the stomach. Both transformations change normal gastric functions, and create abnormal microenvironments with an increased risk for gastric cancer and lymphoma. Own recent investigations indicate, that the distribution and severity of chronic gastritis might be decisively influenced by a rise of antigastric autoimmune reactivity during the H.p. infection. The histologic examination of gastric biopsy samples is essential for an exact diagnosis of the complex pathogenic processes in chronic gastritis. In the future special emphasis of histologic analyses has to be put on the subtypes of gastritis, which are prone for complications and on the evaluation of gastritis remission after H.p. eradication.
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PMID:[Pathology of Helicobacter infection]. 897 54

Helicobacter pylori infection is probably the most common bacterial infection in the world. The pathogenicity of this bacteria has been recognized since 1989 in the developed world where prevalence is 20 to 40%. Its role in gastric and duodenal disease is certain and its low recurrence rate justifies eradication. In the developing world prevalence of Helicobacter pylori infection is over 80% with contamination being maximal in children. Transmission is oro-oral and even feco-oral. Crowded living conditions is the determinant factor. Helicobacter pylori infection exhibits special features in developing world. The prevalence of gastroduodenal disease varies according to geographic area independently of the prevalence of Helicobacter pylori infection and stomach cancer is uncommon. In newborns Helicobacter pylori infection seems to be the primary event for chronic malnutrition and diarrhea syndrome with failure to thrive. In practice detection of Helicobacter pylori is difficult in the developing world and presumptive treatment is always followed by recurrence. In the future active or passive immunization will be the solution.
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PMID:[Helicobacter pylori infection in developing countries]. 928 17

Helicobacter pylori infection and adenomatous polyposis coli (Apc) gene mutations have been linked to gastric cancer in humans, but possible synergistic interaction(s) between these risk factors have not been examined. Fourteen C57BL/6 wild-type and 14 Apc1638 heterozygous mice were inoculated with Helicobacter felis at 6 weeks of age and compared at various time points with a similar number of uninfected control mice of the same genotype. Both infected and uninfected Apc1638 mice had a limited incidence of atypical proliferation foci in the mucosa of the antrum and pyloric junction at 4.5 and 6 months of age, whereas polyps of the antrum and pylorus were present in all mice, regardless of infection status, at 7.5 months. In contrast, no altered gastric mucosal foci were observed in control or infected C57BL/6 mice at any time point. Interestingly, the infected Apc1638 mice had less epithelial proliferation and inflammation in the body of the stomach, lower anti-H. felis serum IgG antibody responses (although both the wild-type and Apc mutant mice had a Th1-like immune response, based on a predominantly IgG2a immunoglobulin response), and higher bacteria and urease scores than did infected wild-type C57BL/6 mice. In conclusion, the Apc1638 truncating mutation leads to gastric dysplasia and polyposis of the antrum and pyloric junction, but H. felis infection of the Apc mutant mouse does not lead to an increased rate of gastric neoplasia. In addition, our data suggest this Apc mutation may actually lead to decreased immune, inflammatory, and gastric hyperplastic responses to Helicobacter infection, suggesting the possibility of a novel role for this tumor suppressor gene in the immune and local tissue responses to gastric bacterial infection.
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PMID:Mice carrying a truncated Apc gene have diminished gastric epithelial proliferation, gastric inflammation, and humoral immunity in response to Helicobacter felis infection. 930 81

Helicobacter pylori infection is a transmissible bacterial infection of the gastric mucosal surface that causes progressive damage with eventual destruction of the stomach. In the United States, the presence of H. pylori infection in patients carries a lifetime risk of developing peptic ulcer of at least 16% and a 1%-3% risk of developing gastric cancer. An infected individual is also a risk to the community because the infection can be transmitted. A review of the data shows that H. pylori is the only treatable infectious disease with such a high rate of morbidity and mortality that is not the subject of an all-out program to eradicate it from the population. The risk of a serious outcome of untreated asymptomatic H. pylori infection is great, or greater, than with asymptomatic syphilis or tuberculosis. H. pylori infection is a serious public health problem, and thus the presence of H. pylori infection justifies treatment. The question is not whom to treat, but whom to test. The gastroenterology community appears to have been unduly influenced by the fact that H. pylori infection is widespread and often asymptomatic, as well as by the costs and complications of current treatment. H. pylori infection is a serious, worldwide infectious disease with tremendous and unacceptable morbidity and mortality. Although there are no emotional reasons to treat H. pylori infection, there are logical and persuasive scientific reasons to treat. If the tools are available, screening the population for the presence of H. pylori infection with the goal of preventing all H. pylori-related diseases is recommended. Our goal should be to totally eliminate H. pylori from the face of the earth, just as we eliminated smallpox.
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PMID:Can therapy even be denied for Helicobacter pylori infection? 939 71

Helicobacter pylori is possibly the most common bacterial infection of humans and is now recognized as the most important acquired cause of peptic ulceration. Epidemiological evidence also recently implicated this bacterium in the pathogenesis of gastric cancer. The mechanism of spread of the organism, by either the faecal-oral or oral-oral route, raises the possibility of transmission of this organism from infected patients to hospital staff particularly those involved in endoscopy. The evidence for an increased risk to endoscopists is contradictory, varying from none to a five-fold increase. This review summarizes the evidence for mode of transmission and risk to hospital staff from this important bacterium.
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PMID:Helicobacter pylori and endoscopy. 1039 31


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