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

Infection with Helicobacter pylori increases an individual's risk of peptic ulceration and gastric cancer. In the developed world, prevalence of infection rises with age and varies with social class. We used a cross-sectional study design to test the hypothesis that H pylori infection would be more closely associated with childhood living conditions than with current socioeconomic status. Prevalence of IgG antibodies against H pylori was determined with an enzyme-linked immunosorbent assay in 215 subjects (median age 46 years, range 18-82) attending a health-screening clinic in London. Seropositivity varied from 9% (age less than 30) to 67% (greater than or equal to 70). Subjects were asked about their living conditions at present and when they were aged 8 years. Absence of a fixed hot-water supply (p = 0.0005) and domestic crowding (p = 0.0005) in childhood were powerful independent risk factors for current infection with H pylori. Among current living conditions, only the number of children living in the household was independently associated with H pylori infection (p = 0.004). Most British adults infected with H pylori probably became infected by household contact in childhood.
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PMID:Childhood living conditions and Helicobacter pylori seropositivity in adult life. 135 29

Disseminated intravascular coagulation (DIC) was examined pathologically in 4906 consecutive autopsy cases during the last 11 years. The cases having pathologically confirmed DIC showing microthrombi in three or more organs were 88. Of the underlying diseases for these cases, malignant tumor was found in 40 cases and diseases of hematopoietic organs in 19. Of the cases with malignant tumor, 11 had gastric cancer, 7 had lung cancer, and 4 had pancreatic cancer. Thirty-three of the 40 cases with malignant tumor showed metastasis in two or more organs. Cases with pathologically confirmed or suspected DIC that had microthrombi in one or more organs were 319. As for the incidence of pathologically suggestive DIC in each disease, the incidence of malignant tumor was 7.3% and that for diseases of the hematopoietic organ was 10.6%. Infection is an important underlying condition, especially gram-negative bacillus septicemia which may play an important role in the development of DIC. An increase in the number of white blood cells appears to be one of the causative conditions of DIC. Kidney is involved most frequently by the deposition of microthrombi, and 27 out of 88 cases show ischemic lesions induced by intravascular coagulation. There were 109 cases having clinically diagnosed or suspected DIC, but 67 cases showed no microthrombus formation. On the other hand, 63 among 4,797 cases with clinically unsuspected DIC revealed microthrombus formation in three or more organs by the postmortem examination.
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PMID:Incidence and clinicopathological significance of DIC in autopsy cases. 666 56

Infection by bacteria, parasites or viruses and tissue inflammation such as gastritis, hepatitis and colitis are recognized risk factors for human cancers at various sites. Nitric oxide (NO) and other oxygen radicals produced in infected and inflamed tissues could contribute to the process of carcinogenesis by different mechanisms, which are discussed on the basis of authors' studies on liver fluke infection and cholangiocarcinoma development. A similar mechanism could apply to other suspected and known cancer-causing agents including Helicobacter pylori infection (stomach cancer) or asbestos exposure (lung mesothelioma). Studies on the type of tissue and DNA damage produced by NO and by other reactive oxygen species are shedding new light on the molecular mechanisms by which chronic inflammatory processes may initiate or enhance carcinogenesis in humans.
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PMID:Chronic infections and inflammatory processes as cancer risk factors: possible role of nitric oxide in carcinogenesis. 751 36

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

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

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 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


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