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

Increased epithelial cell proliferation is associated with an increased risk of gastric carcinoma. Helicobacter pylori infection is an established risk factor for gastric cancer and the organism has recently been classified as a group I carcinogen by an IARC working group. In this study, we describe differences in gastric epithelial cell proliferation between a H. pylori eradicated group (n = 21) and a not eradicated group (n = 8) after anti-H. pylori eradication therapy to show that increased cell proliferation is associated with H. pylori infection. H. pylori infection was determined by rapid urease test and immunohistochemical method with anti-H. pylori polyclonal antibody. Gastric epithelial cell proliferation was assessed using immunohistochemical method using Ki-67 monoclonal antibody. Ki-67 positive cells in H. pylori associated chronic active gastritis were observed in the glandular neck and the upper portion of foveolar epithelium. Patients who cleared their H. pylori infections showed a significant decrease of Ki-67 labeling index after therapy (0.73 +/- 0.10 vs. 0.48 +/- 0.08, p < 0.01). By contrast, Ki-67 labeling index before and after treatment in patients who remained positive for H. pylori showed no significant difference (0.78 +/- 0.08 vs 0.74 +/- 0.10, p > 0.05). These results indicate that H. pylori infection increases the proliferation of gastric foveolar epithelium, which is reduced by the eradication therapy. We suggest that anti-H. pylori eradication therapy can prevent mucosal cell proliferation to be closely associated with gastric carcinogenesis.
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PMID:Decreased gastric proliferation of foveolar epithelial cells after the eradication of Helicobacter pylori. 936

The ideal approach for the initial diagnosis of Helicobacter pylori infection is to perform an endoscopy to obtain biopsy specimens for histology and culture. Histology allows classification of any gastritis lesions present and may have prognostic value, and culture enables susceptibility testing of antimicrobial agents to direct proper treatment. Biopsy specimens must also be taken from the corpus if the patient was pretreated with proton pump inhibitors. The cost of these tests and the delay in receiving results limits their use in clinical practice. Therefore, the urease test, a quick and inexpensive test, is used to detect the presence of H. pylori and constitutes the basic invasive test for H. pylori. A new urease test based on a strip instead of an agar disk may be the test of choice in the future, because of its increased sensitivity and 2-hour delay (instead of 24 hours) in obtaining the result. In some countries, because of the cost, endoscopy will be used in selected patients only, either because of alarm symptoms or age > 45 years, which is considered a threshold for gastric cancer risk. In other patients, the noninvasive tests will be used. The cost of serology makes it more attractive compared with the urea breath test. Currently, there are accurate enzyme-linked immunosorbent assay tests that can be performed in any laboratory and that provide precise and quick diagnoses. In the event of a doubtful result, an immunoblot can be performed, as is the case for other infections. Patient follow-up after treatment provides a different situation because bacterial load is usually lower. A noninvasive test should be performed, and only the urea breath test can be used within the timing originally proposed to test eradication efficacy (i.e., 4-6 weeks after treatment). If the result is positive, susceptibility testing is required before administering a second course of treatment. The increasing use of antimicrobial agents to treat H. pylori is likely to result in antimicrobial resistance, requiring that bacteriologic surveillance programs be implemented. There are numerous research projects ongoing in this area, and one can expect that improved methods, such as colorimetric polymerase chain reaction (PCR) and improved antibody tests, will also be used in the future.
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PMID:How should Helicobacter pylori infection be diagnosed? 939 68

Intestinal metaplasia (IM) appears to be an important stage in the pathogenesis of intestinal type of gastric cancer. The purpose of the study was to evaluate how H. pylori eradication modifies IM in gastric antrum. 35 patients (19 M + 16 F) with peptic ulcer (28 duodenal ulcer +7 gastric ulcer) and antral IM with accompanying H. pylori infection proven by urease test and histological examination were followed-up after healing an ulcer achieved by 14 days treatment with 40 mg/d omeprazole and 2 g/d amoxicillin. Endoscopy examination was done every 4 months during 2 years after eradication. At least two antral biopsies were taken during each endoscopy. H. pylori eradication was achieved in 23 patients (66%). No reinfection was observed during the time of observation. The medium grade of intestinal metaplasia after eradication of H. pylori declined from 1.76 to 0.57 over the period of follow-up (p < 0.01). The difference became statistically significant from the 12 months after eradication. No significant change was seen in the group of non-eradicators (1.83 at the beginning of observation and 1.91 at the end point). Statistical difference between eradicators and non-eradicators was stated from the 12th month after eradication. Total regression of intestinal metaplasia was observed in 30% cases after one year and 61% cases after two years after H. pylori eradication. The cure of H. pylori infection significantly reduces the presence of antral IM. Regression of IM appears to be a long-term process taking many months after H. pylori eradication.
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PMID:Helicobacter pylori eradication and antral intestinal metaplasia--two years follow-up study. 944 62

Many putative virulence determinants of Helicobacter pylori are believed to trigger and worsen the gastroduodenal mucosa damage observed in infected patients. H. pylori urease reacts with the gastric urea and generates ammonia; ammonia combines with water and yields ammonium hydroxide, which is cytotoxic. Ammonia may also inhibit cell proliferation and cause indirect mucosal injury by stimulating neutrophils. Phospholipases may damage the gastric mucosa by degrading phospholipids and generating precursors of ulcerogenic components. Other enzymes, such as protease, neuraminidase, fucosidase, and alcohol dehydrogenase, can contribute to damage of the gastric epithelium by destroying the integrity of mucus or by inducing lipid peroxidation. Infection by vacuolating cytotoxic (VacA+) H. pylori strains is considered to constitute increased risk for development of peptic ulcer and gastric cancer. Exploration of the vacA gene structure has shown the existence of strongly toxigenic strains, and has confirmed at the molecular level the increased ulcerogenic potential of VacA+ H. pylori strains. A pathogenicity island called cag has been recently described in Type 1 H. pylori strains (VacA+/CagA+).cag contains the cagA gene (whose expression is associated with toxigenicity) and many genes, some of which are highly homologous to virulence genes of other virulent bacteria, that account for the enhanced pathogenic potential of CagA+ organisms.
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PMID:Helicobacter pylori factors involved in the development of gastroduodenal mucosal damage and ulceration. 947 42

Helicobacter pylori is present in 40-60% of the population and approximately 10-20% of these infected individuals suffer from a H. pylori associated disease such as peptic ulcer disease or gastric cancer. This article reviews the potential bacterial determinants responsible for and markers predictive of both the acquisition of H. pylori infection and subsequent clinical outcome; i.e., asymptomatic infection or disease. The acquisition of H. pylori infection depends on exposure (hence the increased risk in lower socioeconomic groups and developing nations) to viable bacteria with at least a functional urease gene in a susceptible host. Once infection occurs, bacterial virulence factors, including the vacuolating cytotoxin, and genes of the cag pathogenicity island, as well as nonbacterial factors may determine disease outcome. Future research is being directed at discovering other bacterial virulence factors responsible for the different clinical outcomes of H. pylori infection. This will be greatly enhanced by the recent release of the complete genome sequence of H. pylori. The determination of the relative importance of each of these recognized and other as yet unrecognized factors responsible for disease outcome will assist in the appropriate targeting of patients in the treatment of H. pylori infection.
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PMID:A review of the possible bacterial determinants of clinical outcome in Helicobacter pylori infection. 960 5

One hundred and twenty consecutive patients above 12 years of age with dyspepsia were studied from June 1993 to September 1994. They underwent upper gastrointestinal endoscopy to find the mucosal lesions which were associated with their dyspeptic symptoms. At endoscopy gastric mucosal biopsies were taken in order to identify Helicobacter pylori (H. pylori) using three different techniques: culture, histology and the rapid urease test. Normal looking mucosa was the commonest single endoscopic finding, accounting for 34.2%, followed by gastritis 31.7% and duodenal ulcer 29.2%. However, when duodenal ulcers and gastric ulcers were put together, then peptic ulcer was the most prevalent finding accounting for 38.4%. Peptic ulcer was the most prevalent pathological finding in both young (less than 50 years) and older patients (50 years and above). Duodenal ulcer was more prevalent than gastric ulcer in the younger age group with a ratio of 5.8:1, however, the ratio in the older age group was 1:1. Gastric cancer was only found in patients aged 50 years and above, accounting for 17.4% of dyspeptic symptoms in this age group. Females were found to have more normal endoscopic findings than males (59.6%, versus 17.8% respectively). The difference being statistically significant (p < 0.001). All our cases of peptic ulcer disease had evidence of H. pylori infection while dyspeptic patients with normal endoscopic mucosal findings had H. pylori in 80.5% of cases. The difference in prevalence of H. pylori in the two groups was statistically significant (p < 0.001). Surprisingly, evidence of H. pylori in gastric cancer cases was very low in this study, being found in only 25% of patients.
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PMID:Endoscopic findings and prevalence of Helicobacter pylori in Kenyan patients with dyspepsia. 964 Aug 29

Helicobacter pylori, one of the most prevalent human pathogens, is associated with chronic gastritis, peptic ulcer disease, and possibly gastric cancer and primary gastric lymphoma. The need to treat these patients has necessitated the development of improved methods to diagnose H. pylori infection. We present the preliminary assessment of a 13C-urea breath test (UBT) in which the expired 13CO2 is detected in a rapid, simple, inexpensive way by the LARA (Laser Assisted Ratio Analyzer) System (Alimenterics, Inc., Morris Plains, NJ). Eighty-seven consecutive patients, examined for upper gastrointestinal symptoms, underwent endoscopy. H. pylori infection was established by antral biopsies and a rapid urease test (CLOtest). The UBT was performed between 2 and 24 hours after endoscopy. Of the 84 analyzable patients, 70 were found to be H. pylori-positive either by histology or by CLOtest. All 70 were positive by the LARA UBT, yielding a sensitivity of 100%. Fourteen patients were negative for H. pylori by histology and the CLOtest. Of these, 12 were negative by the LARA UBT and 2 were positive, yielding a specificity of 85.7%; because of the limitations of H. pylori detection by histology or urease assays, however, the specificity of the UBT may have been underestimated. Our study demonstrates the feasibility of a nonradioactive, rapid UBT based on the LARA system and suggests the need for its more detailed evaluation.
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PMID:A simplified urea breath test for the diagnosis of Helicobacter pylori infection using the LARA System. Laser Assisted Ratio Analyzer. 964 7

Gastric adenocarcinoma is the most prevalent cancer in South Korea, and Helicobacter pylori (H. pylori) infection is also common. This study was performed to examine the association between H. pylori infection and gastric cancer, taking into account various other factors. To investigate the association between gastric adenocarcinoma and H. pylori infection, determined by urease-positive reaction in the CLO test, a total of 175 paired specimens (175 tumor and 175 tissues adjacent to tumor) of stomach cancer patients and a total of 113 control specimens were obtained. The positive H. pylori infection rates were 78.9% (138/175) among the patients in specimens of tumor or tissues adjacent to the tumor and 41.6% (47/113) among controls in the CLO test. A positive correlation between H. pylori infection and gastric cancer was observed (age-adjusted odds ratio, 7.0; MH chi2=34.5 with P<0.0005). These data suggest that stomach cancer patients in Korea have high infection rates of H. pylori regardless of site specificity, and this infection might be causally associated with stomach cancer.
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PMID:Association of Helicobacter pylori infection with gastric adenocarcinoma. 970 56

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

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


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