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

Recent epidemiologic evidence indicates that Helicobacter pylori infection increases the risk for gastric carcinoma. Infection with H. pylori leads to chronic gastritis, which usually persists for life unless treated with antimicrobial drugs. Because the great majority of gastritis patients never develop neoplasias, research concerning those who do may provide clues about carcinogenesis. In affluent populations, H. pylori infection leads to nonatrophic gastritis, predominantly involving diffusely the antrum (diffuse antral gastritis), the basic lesion seen in patients with duodenal ulcer, which has not been associated with increased risk for gastric carcinomas. In populations with high gastric cancer risk, H. pylori infection is associated with multifocal atrophic gastritis, which frequently advances to intestinal metaplasia, occasionally to dysplasia, and rarely to carcinoma. H. pylori infection increases the rate of proliferation of the gastric epithelial cells and decreases the gastric secretion of ascorbic acid, processes that may modulate the process of carcinogenesis. Infection with H. pylori is characterized by infiltration of lymphocytes, polymorphonuclear leukocytes, and macrophages in the gastric mucosa. There is considerable interest in investigating oxygen radicals originating in white blood cells and the possibility that they induce mutations with carcinogenic potential in the gastric epithelium.
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PMID:Helicobacter pylori and gastric carcinogenesis. 776 38

In patients with systemic sclerosis peristaltic abnormalities may delay gastric emptying, giving rise to bacterial overgrowth, including possibly Helicobacter pylori (HP). Infection with Helicobacter is an important risk factor for esophageal and gastric diseases, including esophagitis, gastritis and gastric cancer. The purpose of this prospective study was to assess gastric HP infection in patients with systemic sclerosis. In 12 patients with systemic sclerosis the newly introduced breath test with 13C-labelled urea was used for indirect detection of gastric urease activity due to HP infection. Five out of 12 patients gave Helicobacter-positive results (42%); 7 patients were negative for Helicobacter colonization (58%). Thus, the risk for gastric diseases caused by HP infection is enhanced in patients with systemic sclerosis compared with white healthy, asymptomatic persons examined in other studies. Helicobacter-positive patients were treated with 2 x 20 mg omeprazole and 4 x 500 mg amoxicillin over 14 days. Afterwards the 13C-urea breath test was repeated and showed negative results for Helicobacter in all systemic sclerosis patients treated. Dual therapy with omeprazole and amoxicillin therapy effectively eradicated HP. The 13C-urea breath test did not cause any side-effects and is therefore considered to be a non-invasive, non-toxic and safe method for the diagnosis and therapeutic control of Helicobacter-status.
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PMID:Helicobacter pylori in patients with systemic sclerosis: detection with the 13C-urea breath test and eradication. 781 72

Gastroduodenal infection by Helicobacter pylori is a known cause of many gastric and duodenal disorders. Infection by H. pylori is very frequent ant its prevalence increases with age by about 1% per year. Human-to-human transmission appears probable. H. pylori lives under the mucous layer of gastric-type epithelium. It is the main causal agent of chronic diffuse superficial gastritis (type B). After several decades lesions of superficial gastritis can evolve to atrophic gastritis. Spontaneous short- or long-term disappearance of H. pylori from the antral mucosa is rare. H. pylori infection appears to be necessary for the recurrence of duodenal as well as gastric ulcer. Eradication decreases the frequency of relapses, but its long-term effect remains to be evaluated. The presence of H. pylori, however, is not itself sufficient for ulcer development. Why only some patients infected with H. pylori develop ulcer has not been elucidated. The role of H. pylori infection in the gastrotoxicity of non-steroid anti-inflammatory agents is still debated. It has not yet been determined whether eradication leads to reduction of the high digestive morbidity linked to intake of such agents, but it is known that eradication of H. pylori does not obviate the risk of ulcer and of complication. There is a significant association between H. pylori infection, atrophic gastritis and intestinal type gastric cancer. H. pylori infection appears to be one of the factors in gastric cancerogenesis. Cellular proliferation of gastric lymphomas to low-grade B cells would in most cases be secondary to chronic H. pylori infection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Helicobacter pylori and gastroduodenal disease]. 793 99

The addition of 5 years of follow-up and over 411,000 person-years of observation to a cohort of 34,081 men and women employed in U.S. furniture and other related industries allowed the investigation of mortality patterns among women and minority races in addition to white men. A significant excess of pleural mesotheliomas occurred among white men (standardized mortality ratio [SMR] = 3.7, 95% confidence interval [CI] = 1.2-8.7) but could not be linked to a particular type of furniture manufacturing. SMRs for myeloid leukemia and chronic nephritis were elevated among white men employed in the wood furniture industry but were not statistically significant. Males in the black/other race categories in wood furniture plants showed nonsignificant mortality excesses for infectious diseases and cancers of the prostate and colon and rectum. Among white women employed in wood furniture plants, mortality was elevated for cancers of the pancreas and lung during the most recent follow-up period. In metal furniture plants, mortality was raised among men in both race groups for kidney cancer (black/other SMR = 8.0, 95% CI = 1.6-23.2; white SMR = 2.1, 95% CI = 0.4-6.2) and diabetes mellitus (black/other SMR = 2.2, 95% CI = 0.6-5.6; white SMR = 1.8, 95% CI = 0.7-3.9). Stomach cancer mortality was significantly elevated (SMR = 3.3, 95% CI = 1.3-6.8) among white men in metal furniture plants and was of the same magnitude over both the previous and the most recent follow-up periods. Among those working with textiles, SMRs were significantly elevated for leukemia (SMR = 6.1, 95% CI = 1.2-7.8) and cancers of the colon and rectum (SMR = 3.2, 95% CI = 1.3-4.5) for white women. Lung cancer mortality was increased for white men and women in textile operations, but SMRs were not statistically significant. SMRs for a number of other causes of death that were elevated at the end of the earlier follow-up period were not increased during the new follow-up period.
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PMID:Extended mortality follow-up among men and women in a U.S. furniture workers union. 801 Feb 96

H. pylori is the major cause of gastritis in children and adults. Studies in children have demonstrated a specific association between H. pylori and primary gastritis. H. pylori colonization of the gastric mucosa is also important in relation to the natural history of duodenal ulcer disease. Duodenal ulcers do not appear to relapse if H. pylori is cleared from the gastric mucosa. Because of the low incidence of duodenal ulcer disease in children, a multicenter study is required to demonstrate whether this finding is true in children. To date, no specific symptoms have been associated with the presence of H. pylori gastritis in children. H. pylori gastritis may therefore be an asymptomatic condition in the majority of infected children. Further studies in relation to H. pylori gastritis and symptoms in children will be important because it should be easier to identify specific symptoms in children than in adults. H. pylori gastritis in children can be diagnosed by obtaining antral biopsy specimens for culture and histologic study during upper gastrointestinal endoscopy. Serologic study is also a sensitive and specific indicator of H. pylori infection, provided that children's sera are used to standardize the assay. Noninvasive tests such as 13C urea breath tests are very attractive for use in children but are expensive. H. pylori can be cleared from the gastric mucosa in as many as 70% of children by using a combination of metronidazole or amoxicillin with colloidal bismuth subcitrate or bismuth subsalicylate. Studies in children are important in determining the epidemiology of H. pylori. Children in Western societies are not usually colonized. Infection becomes more common with increasing age. Children in underdeveloped countries and those living in poor social conditions in Western countries are much more likely to be infected at a young age. The reason for the increased prevalence of infection among these groups is not known. There is also significant intrafamilial clustering of H. pylori infection. Again, it is unclear why the organism is clustered within households and institutions. Future studies on children will be of importance in determining whether H. pylori gastritis is a cause of specific symptoms, the epidemiology of H. pylori infection, and the possible role of the organism in the natural history of gastric cancer.
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PMID:Helicobacter pylori in the pediatric patient. 844 65

In 1985, gastric cancer was the second most common cause of cancer death in the world. The rapid decline in gastric cancer rates over the last few decades has been attributed to a decline in the prevalence of environmental risk factors for gastric cancer and/or an increase in the prevalence of protective factors. One such risk factor could be the bacterium Helicobacter pylori. Epidemiological studies have shown that areas with high gastric cancer rates often have a correspondingly high prevalence of H. pylori and prospective studies have shown that subjects with serological evidence of H. pylori infection were significantly more likely to go on to develop gastric cancer than those who did not. Helicobacter pylori itself does not appear to be either genotoxic or mutagenic. Infection is, however, associated with increased cell turnover, a chronic immune response accompanied by increased levels of reactive oxygen metabolites and a reduction in gastric levels of ascorbic acid, all conditions that could favour the development of cancer. Nonetheless, the majority of those who are infected with H. pylori do not go on to develop gastric cancer and other factors, such as the strain of the infecting organism or consumption of dietary antioxidants including vitamin C, could also affect the risk of cancer. Finally, it has been estimated that more than one third, and possibly as many as 90% of gastric cancers might be attributable to infection with H. pylori. Prevention and treatment of infection are, therefore, possible approaches to reducing gastric cancer rates. It is, however, unclear what, if any, effect eradication of the infection would have on an individual's risk of gastric cancer and, to date, anti-Helicobacter therapy has only been shown to be of potential benefit in the treatment of low grade gastric MALT lymphomas.
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PMID:Helicobacter pylori as a risk factor for cancer. 856 54

Helicobacter pylori (H. pylori) is responsible for one of the most frequently encountered infectious diseases worldwide. H. pylori infection can lead to the development of gastritis and peptic ulcer disease. The presence of H. pylori in the human stomach also represents an increased risk for gastric cancer and gastric lymphoma. Epidemiologic data obtained in adults suggest that the actual colonization with H. pylori is in fact determined by childhood factors. Therefore, the pediatric age group represents the ideal target population for studies concerning the pathogenesis and epidemiology of H. pylori infection.
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PMID:Helicobacter pylori disease in childhood. 866 50

Helicobacter pylori is an important pathogen in humans, causing chronic gastritis and playing a major role in the development of peptic ulcers and gastric cancer. The organism is highly adapted to the human stomach, largely due to its motility and ability to produce large amounts of urease. It binds specifically to the gastric mucosa via adhesion pedestals; colonization of the duodenum only occurs in the presence of gastric metaplasia. Infection with H. pylori leads to gastritis, but the majority of infected patients are asymptomatic, and it is thought that the ability of H. pylori to cause more severe disease may be related to the presence of the cagA gene. With improvements in public health and living conditions, the prevalence of H. pylori infection in developed countries is decreasing, and this is associated with a decline in the incidence of peptic ulcer and gastric cancer.
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PMID:The nature of Helicobacter pylori. 872 98

Helicobacter pylori is firmly established as a human pathogen; it fulfils all of Koch's postulates as the infectious agent causing chronic, active (type B) gastritis. Infection is strongly associated with duodenal and gastric ulcer. Recently, gastric mucosal-associated lymphoid tissue lymphoma has been successfully treated by curing H. pylori infection. Because of the evidence that the organism causes chronic gastritis and an increased risk of gastric cancer, it has been classified as a category 1 carcinogen by the World Health Organization. However, the overwhelming majority of people infected have no symptoms. Current eradication therapy is not ideal; there are treatment failures and substantial side effects. As a result, therapy should be reserved for people with clinical symptoms and complications. The infection, if present, should be treated in patients who have endoscopic evidence of mucosal ulcers in the stomach or duodenum. Current evidence does not support treating the infection to prevent gastric carcinogenesis or to alleviate symptoms of abdominal discomfort in the absence of peptic ulcers.
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PMID:Why guidelines are required for the treatment of Helicobacter pylori infection in children. 888 75

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


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