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

Gastric cancer is two to four-fold more common in Maori and Pacific Island ethnic groups compared with Europeans. This study aimed to determine if intestinal metaplasia was more common in these ethnic groups. Patients attending for endoscopy for dyspepsia had six biopsies to determine the presence of Helicobacter pylori by at least two of the following tests: rapid urease test, 13C urea breath test, culture of histology and the presence, extent and subtypes of intestinal metaplasia. Biopsies were taken from 158 patients: Europeans (42%), Maori (23%), Pacific Islanders (35%). Helicobacter pylori and intestinal metaplasia were detected in 88 and 60% of Maori/Pacific Island patients, respectively, and 47 and 29% of Europeans, respectively. Type I intestinal metaplasia was detected in 43% of all patients, type II (26%) and type III (7.0%). The mean age of Maori/Pacific Island patients with intestinal metaplasia and type III intestinal metaplasia was 53 and 51 years respectively, compared with Europeans aged 65 and 72 years. Univariate analysis showed that intestinal metaplasia was associated with ethnicity and H. pylori (P < 0.001) but not age, smoking, endoscopic diagnosis or gender. Intestinal metaplasia is more common and occurs at an earlier age in Maori and Pacific Island patients.
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PMID:Intestinal metaplasia subtypes and Helicobacter pylori infection: a comparison of ethnic groups in New Zealand. 971 96

Since Helicobacter pylori was first isolated by Warren and Marshall in 1983, many investigators have reported that it is closely associated with gastro-duodenal diseases. Several diagnostic methods, C-urea breath tests, rapid urea test, histological exam and culture, are used for detecting H. pylori. Japanese monkey and Mongolian gerbils is the animal model that can sustain persistent colonization with H. pylori. Japanese monkeys persistently infected with H. pylori can develop histological gastritis quite similar to that in humans. Eradicating H. pylori markedly reduces the recurrence of peptic ulcers. The new triple therapy regimen consisting of proton pump inhibitor (PPI) plus two antibiotics is effective for eradicating H. pylori. This therapy has shown high rates of H. pylori eradication (90%) with few side effects. An increase in the prevalence of antibiotic-resistant H. pylori strains has been reported worldwide. Failed attempts to eradicate the bacteria resulted in an increased number of H. pylori resistant strains. The relationship between H. pylori infection and gastric cancer has been recently investigated.
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PMID:[Helicobacter pylori infection]. 972 27

While European and United States guidelines for the management of Helicobacter pylori infection have been developed, there are no guidelines for the Asian Pacific. International experts and recognised local authorities met in Singapore in 1997 to develop appropriate guidelines, taking into account the high background prevalence of infection, high incidence rates of gastric cancer and resource limitations. Recommendations were made based on randomised controlled trials or where this was not possible, they were based on the current best available evidence or on good clinical practice. A number of acceptable diagnostic tests for infection are available throughout the region. The non-endoscopic methods of choice are the urea breath test or a locally validated antibody test. If endoscopy was to be performed, a biopsy urease test was recommended as the test of first choice, with histology recommended only if this was negative. Post treatment testing was not recommended for all patients; a urea breath test was considered the test of choice if available. All gastric and duodenal ulcer patients who are infected with H. pylori should be treated for H. pylori whether the ulcer is active or in remission. Patients requiring long term non-steroidal anti-inflammatory drug therapy who have a current or recent history of dyspepsia, patients with early gastric cancer or low grade gastric mucosa associated lymphoid tissue lymphoma, and patients with a family history of gastric cancer should be treated. However, it was concluded that there wasn't sufficient evidence that cure of H. pylori infection reduces the risk or prevents the development of gastric adenocarcinoma. Many patients with dyspepsia in the region will request or require early upper endoscopy because of an inherent fear of gastric cancer. However, where endoscopy is not available or is too costly, alternative acceptable approaches were recommended in high risk cancer regions. While evidence is inconclusive to support treatment of H. pylori infection in non-ulcer dyspepsia, it was agreed that treatment be offered to patients with documented infection on a case-by-case basis. Treatment regimens need to attain an eradication rate of 90% or greater by per protocol analysis and 80% or greater by intention-to-treat analysis. A number of 7-day regimens were recommended based on available evidence. These regimens were considered likely to maximize the chances of successful eradication with one course of treatment, thereby reducing the risk of acquired antibiotic resistance and leading to long term cost savings.
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PMID:Report of the 1997 Asia Pacific Consensus Conference on the management of Helicobacter pylori infection. 973 64

An algorithmic approach to evaluation of dyspepsia or abdominal discomfort begins with differentiation between peptic ulcer disease and gastroesophageal reflux disease as well as recognition of alarm signs and symptoms for gastric cancer, which are indications for early endoscopy. In the absence of alarm symptoms, most patients should undergo noninvasive testing for H pylori infection with a serologic, urea breath, or stool antigen test. Factors to consider in selection of appropriate testing include reliability, specificity, sensitivity, cost, and local access and expertise. As a general rule, physicians should choose a test that has the best accuracy for the level of testing expertise available. The basic principle underlying testing for H pylori is that patients should not undergo testing unless the physician is willing to treat on the basis of a positive test result. In patients who receive treatment, confirmation of cure is important for preventing further morbidity and reducing risk of transmission of infection.
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PMID:Recognizing peptic ulcer disease. Keys to clinical and laboratory diagnosis. 1008 37

Helicobacter pylori is the causative agent of most cases of gastritis. Once acquired, H. pylori establishes chronic persistent infection; it is this long-term infection that, is a subset of patients, leads to gastric or duodenal ulcer, gastric cancer or gastric MALT lymphoma. All fresh isolates of H. pylori express significant urease activity, which is essential to survival and pathogenesis of the bacterium. A significant fraction of urease is associated with the surface of H. pylori both in vivo and in vitro. Surface-associated urease is essential for H. pylori to resist exposure to acid in the presence of urea. The mechanism whereby urease becomes associated with the surface of H. pylori is unique. This process, which we term "altruistic autolysis," involves release of urease (and other cytoplasmic proteins) by genetically programmed autolysis with subsequent adsorption of the released urease onto the surface of neighboring intact bacteria. To our knowledge, this is the first evidence of essential communal behavior in pathogenic bacteria; such behavior is crucial to understanding the pathogenesis of H. pylori.
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PMID:Structure, function and localization of Helicobacter pylori urease. 1037 51

To characterize chemical carcinogens in acidic-nitrosated fish sauce sample, N-nitrosamides in the sample were separated by two kinds of reversed-phase HPLC columns, and with detection by photolysis-pyrolysis-thermal energy analyzer. A strong chromatographic peak at t(R) 12 or 4.5 min, same as that for N-(nitrosomethyl)urea (NMU), was obtained on PRP-1 or C(18) HPLC column from fish sauce sample with 10 mM trifluoroacetic acid as the basic mobile; acetonitrile, as organic modifier after the sample was nitrosated by 5 mmol/L of sodium nitrite (final concentration) at 37 degrees C and pH 2.0 for 1 h. No response above t(R) could be observed from the nitrosated sample in the detection system without photolysis. Such a peak could not be obtained from the unnitrosated fish sauce either. These results indicated that the component was NMU. Furthermore, this component, NMU, could also be detected in the nitrosated human gastric juice sample spiked with fish sauce. The formation of NMU in the sample was pH- and nitrite-dependent. This paper provides direct evidence that NMU formation could occur in fish sauce from the high-risk area for stomach cancer and in the fish sauce spiked human gastric juice during nitrosation under simulated gastric conditions.
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PMID:Characterization of N-(Nitrosomethyl)urea in Nitrosated Fermented Fish Products. 1055 19

Numerous epidemiological studies demonstrated the association between Helicobacter pylori (H. pylori) infection and gastric cancer but the mechanism of the involvement of H. pylori in gastric cancerogenesis remains virtually unknown. This study was designed to determine the seropositivity of H. pylori and cytotoxin associated gene A (CagA), serum gastrin and gastric lumen gastrin levels under basal conditions and following stimulation with histamine in gastric cancer patients and controls. 100 gastric cancer patients aging from 21 to 60 years and 300 gender- and age-adjusted controls hospitalized with non-ulcer dyspepsia (NUD) entered this study. 13C-Urea Breath Test (UBT), serum immunoglobulin (IgG) antibodies to H. pylori and CagA were used to assess the H. pylori infection and serum levels of IL-1beta, IL-8 and TNFalpha were measured by enzyme-linked immunosorbent assay (ELISA) to evaluate the degree of gastric inflammation by H. pylori . Gastrin-17 mRNA and gastrin receptors (CCK(B)) mRNA expression in gastric mucosal samples taken by biopsy from the macroscopically intact fundic and antral mucosa as well as from the gastric tumor was determined using RT-PCR. The overall H. pylori seropositivity in gastric cancer patients at age 21-60 years was about 92%, compared, respectively, to 68%, in controls. A summary odds ratio (OR) for gastric cancer in H. pylori infected patients was about 5.0 . The H. pylori CagA seropositivity in gastric cancer patients was about 58.5% compared to 32.4% in controls, giving the summary OR for gastric cancer in CagA positive patients about 8.0. The prevalence of H. pylori- and H. pylori CagA-seropositivity was significantly higher in cancers than in controls, irrespective of the histology of gastric tumor (intestinal, diffuse or mixed type). Median IL-1beta and IL-8 reached significantly higher values in gastric cancer patients (9.31 and 30.8 pg/ml) than in controls (0.21 and 3.12, respectively). In contrast, median serum gastrin in cancers (as total group) was several folds higher (62.6 pM) than in controls (19.3 pM). Also median luminal gastrin concentration in gastric cancer patients was many folds higher (310 pM) than in controls (20 pM). This study shows for the first time that cancer patients are capable of releasing large amounts of gastrin into the gastric lumen to increase luminal hormone concentration to the level that was recently reported to stimulate the growth of H. pylori. There was no any correlation between plasma gastrin levels and gastric luminal concentration of gastrin suggesting that: 1) luminal gastrin originates from different source than plasma hormone, most probably from the cancer cells, 2) cancer cells are capable of expressing gastrin and releasing it mainly into the gastric juice and 3) the gastric cancer cells are equipped with gastrin-specific (CCK(B)) receptor so they exhibit the self-growth promoting activity in autocrine fashion. This notion is supported by direct detection of gastrin mRNA and gastrin receptor (CCK(B)-receptors) mRNA using RT-PCR in cancer tissue. To our knowledge this is the first study showing an important role of gastrin as self-stimulant of cancer cells in patients infected with H. pylori. Basal and histamine maximally stimulated acid outputs were significantly lower in gastric cancer patients than in controls despite of enhanced gastrin release, particularly in cancer patients and this might reflect the mucosal inflammatory changes (increased serum levels of proinflammtory interleukins - IL-1beta and IL-8), that are known to increase gastrin release. We conclude that: 1) H. pylori infected patients, particularly those showing CagA-seropositivity, are at greatly increased risk of development of gastric cancer, 2) H. pylori-infected cancer patients produce significantly more IL-1beta and IL-8 that might reflect an H. (ABSTRACT TRUNCATED)
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PMID:Role of gastrin in gastric cancerogenesis in Helicobacter pylori infected humans. 1069 65

Microsatellite markers permit the analysis of microsatellite instability and loss of heterozygosity. Frequently, the allelotypes of microsatellites are interpreted in the presence of numerous bands in gels. The importance of different gel electrophoresis conditions in the interpretation of microsatellite patterns was tested. Microsatellite markers were used to amplify DNA from gastric cancer samples and adjacent gastric mucosa. Polymerase chain reaction (PCR) products were separated by electrophoresis through 7% polyacrylamide gels containing either 5.6 M urea and 32% formamide or 7 M urea. PCR reactions separated on urea/formamide gels resulted consistently in clear allele definition (one or two bands), whereas 7 M urea gels resulted in allele patterns that comprised multiple bands. Analysis of microsatellite abnormalities using nonformamide gels gave false negative results in just under a third of cases (four of 13). In conclusion, the interpretation of microsatellite alterations in cancer DNA is improved by using electrophoresis conditions that result in complete DNA denaturation, such as urea/formamide/acrylamide gel electrophoresis.
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PMID:Variability in the interpretation of microsatellite patterns with different electrophoretic conditions. 1074 82

In-depth meetings of the XIth International Workshop on Gastroduodenal Pathology and Helicobacter pylori led to the presentation and discussion of extensive new data on H. pylori and its diseases. The mode of transmission of H. pylori remains unclear, and it remains unknown why only a small proportion of infected individuals develop duodenal or gastric ulcer disease and even fewer develop gastric cancer. The role of H. pylori eradication in persons with uninvestigated dyspepsia remains controversial. New clinical trials of H. pylori treatment show symptom relief and improvement in the quality of life of persons with functional dyspepsia, especially in those with ulcer-like or reflux-like dyspepsia. Clearly the move is toward symptom-based management of persons with dyspepsia, with fewer endoscopies being needed in the otherwise healthy young dyspeptic patients. It remains controversial whether eradicating H. pylori in duodenal ulcer or functional dyspepsia increases the risk of subsequent development of gastroesophageal reflux disease. The one-week proton pump inhibitor-based triple regimens remain the gold standard of H. pylori therapy, but some of the ranitidine bismuth citrate plus two antibiotic regimens also achieve an 80% H. pylori eradication rate on an intention-to-treat basis. While the urea breath test remains the noninvasive test of choice, interesting new data are available on the use of stool antigen testing to diagnose H. pylori infection. The number of H pylori-associated gastroduodenal diseases grows to include possible liver, vascular, immune and skin conditions.
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PMID:From bench to bedside to bug: an update of clinically relevant advances in the care of persons with Helicobacter pylori- associated diseases. 1075 16

Helicobacter pylori (H. pylori) infection is acquired in childhood, earlier in developing countries, as a consequence the prevalence of infection is higher in developing countries (70%) than in developed countries (5-15%). H. pylori infection spreads from person-to-person, however the precise mode of transmission (oral-oral, fecal-oral or gastro-oral routes) is as yet, not known. Diagnosis of H. pylori infection can be performed with both invasive endoscopic-based tests, or non-invasive tests, mainly by measurement of IgG antibodies against the bacterium in serum samples or by measurement of 13CO2 in expired air (13C-urea breath test). In clinical practice endoscopy and biopsy is recommended before treatment to determine the presence and the degree of gastritis or ulcer. However, endoscopy is a complicated procedure in children and diagnosis of infection can be based on a non-invasive test. The association of H. pylori infection with recurrent abdominal pain seems evident in a subgroup of children with endoscopic features of gastritis, ulcer or hemorrhage. There is an increasing interest in the extraintestinal manifestations of H. pylori infection in children, i.e. iron-deficiency anemia, growth retardation and migraine, but this domain remains controversial. Since infection at a young age is believed to result in chronic atrophic gastritis and gastric cancer in adult life, it is logical to consider a future massive programme of eradication and immunization. Regimens suggested for H. pylori eradication are a combination of inhibitors of gastric acid secretion plus two antibiotics for 7-10 days.
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PMID:[Helicobacter pylori infection in pediatrics. Present knowledge and practical problems]. 1082 91


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