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

Helicobacter pylori has been shown to be the cause of chronic active gastritis and the evidence that it is involved in the development of peptic ulcer disease and gastric cancer is compelling. Narrow host range, tissue specificity, and chronic inflammation are hallmarks of infection. The study of virulence determinants has just begun but it seems likely that urease, adhesins, cytotoxins, and mediators of inflammation will prove to be important.
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PMID:Helicobacter pylori and gastroduodenal disease: pathogenesis and host-parasite interaction. 134 68

Helicobacter pylori (HP) has been shown to possibly be a pathogen of gastric carcinoma. HP has urease activity and produces ammonia in the stomach. In this study, the role of ammonia on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were investigated in rats. After 24 weeks pretreatment with MNNG (83 mg/l), 0.01% ammonia or tap water as a drinking water was administered for 24 weeks. The ammonia-treated rats showed a significantly higher incidence of gastric cancer (percent of animals with tumors and number of tumors per rat). Ammonia would thus appear to have an important role in HP-related human gastric carcinogenesis.
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PMID:Ammonia: a possible promotor in Helicobacter pylori-related gastric carcinogenesis. 151 5

The association between Helicobacter pylori, gastritis, and peptic ulcer is well established, and the association of infection with gastric cancer has been noted in several developing countries. However, the pathogenic mechanism(s) leading to disease states has not been elucidated. The H. pylori urease is thought to be a determinant of pathogenicity, since the enzyme is produced by all H. pylori clinical isolates. Evidence indicates that some H. pylori strains are more cytotoxic than others, with a correlation between the activity of the urease and the presence of a vacuolating cytotoxin having been made. However, the number of cytotoxins remains unknown at this time. The relationship between the urease and cytotoxicity has previously been examined with chemical inhibitors. To examine the role of the urease and its relationship to cytotoxicity, urease-deficient mutants were produced following ethyl methanesulfonate mutagenesis of H. pylori 87A300. Two mutants (the ure1 and ure5 mutants) which were entirely deficient in urease activity (Ure-) were selected. Characterization of the isolates at the protein level showed that the urease subunits lacked the ability to complex and form the active urease enzyme. The ure1 mutant was shown to be sensitive to the effects of low pH in vitro and exhibited no cytotoxicity to eucaryotic cells, whereas the parental strain (Ure+) produced a cytotoxic effect in the presence of urea. Interaction between the H. pylori Ure+ and Ure- strains and Caco-2 cells appeared to be similar in that both bacterial types elicited pedestal formation and actin condensation. These results indicate that the H. pylori urease may have many functions, among them (i) protecting H. pylori against the acidic environment of the stomach, (ii) acting as a cytotoxin, with human gastric cells especially susceptible to its activity, and (iii) disrupting cell tight junctions in such a manner that the cells remain viable but an ionic flow between the cells occurs.
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PMID:Characterization of Helicobacter pylori urease mutants. 156 78

Helicobacter pylori infection is now recognized as the primary cause of active chronic gastritis in humans. Most infected persons remain asymptomatic, but are at increased risk for the development of peptic ulcer disease and possibly gastric cancer. The pathogenesis of this infection is not well understood, but motility and urease activity are virulence factors in an animal model. The eradication of H. pylori infection is associated with resolution of gastritis and a decreased rate of duodenal ulcer recurrence.
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PMID:Helicobacter pylori and gastroduodenal disease. 158 May 78

Colonization by Helicobacter pylori (HP) in 53 patients after remote gastric surgery and Roux-en-Y anastomosis was investigated using a rapid urease test (CU-Test) and histology (H&E and Giemsa stain). The pH-value of gastric juice was measured. HP infection of the gastric remnant was found in 56% of 43 patients after partial resection and in no case after total gastric resection. HP-positive and HP-negative patients were comparable in age, sex distribution, indication and technique of gastric operation (except for total gastrectomy with jejunal gastric replacement), intake of acid inhibiting drugs and antibiotics was well as in the presence or absence of a macroscopically visible pathology of the gastric mucosa. On the other hand, the two groups differed in their histological findings, pH-value of gastric juice and time interval since surgery. HP infection of gastric remnants is associated with significant glandular atrophy and an additional rise in gastric intraluminal pH compared with HP-negative patients. Both changes may involve an increased risk for gastric cancer. In this report on patients with Y-en-Roux operation there is no decrease in gastric HP-colonization with an increasing interval since the time of operation, but rather an increase. This phenomenon seems to depend on the absence of enterogastric reflux.
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PMID:[Helicobacter pylori colonization of the gastric remnant following partial resection]. 162 50

20 H. pylori-positive patients with gastric or duodenal ulcer disease (n = 16, one with proof of gastric cancer obtained by histology) or severe non-ulcer dyspepsia (n = 4) were entered in a pilot study to examine the effect of a combination of omeprazole (40 mg) before breakfast and ciprofloxacin (2 x 500 mg) 1 hour after meals for 1 week to treat Helicobacter pylori (Hp). The eradication rate was 15% (3 out of 20 patients) 4 weeks after therapy. Ulcer healing occurred in 2 of 3 patients having eradication and 9 of 11 control patients with positive H. pylori urease test and/or culture 4 weeks after treatment. Despite some good theoretical background, this drug combination is inefficient to eradicate H. pylori and cannot be recommended for routine clinical practice. No major side effects of the therapy-regimen were observed.
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PMID:[Ciprofloxacin-omeprazole combination therapy for eradication of Helicobacter pylori]. 186 70

A causative role is now accepted for Helicobacter (formerly Campylobacter) pylori in type B gastritis, and evidence is accumulating that H. pylori infection plays a major contributory role in duodenal ulcer, gastric ulcer, and epidemic gastric cancer. The prevalence of H. pylori in any population remains unknown. We compared the prevalence of H. pylori infection in the Riyadh region of Saudia Arabia, using a specific and sensitive ELISA for IgG antibody against the high molecular weight cell-associated antigen of H. pylori (urease). Subjects were interviewed, demographic data were collected, and a serum sample was obtained. Subjects completed a questionnaire that included questions about level of education, smoking, medications used, presence and frequency of symptoms referable to the upper gastrointestinal tract, and family history of ulcer disease. We studied 557 individuals (ranging in age from 5 to 91 yr). The prevalence of H. pylori infection increased rapidly with age: from 40% of those ages 5-10 yr, to more than 70% of those 20 or older. H. pylori infection occurred with significantly more frequency in adults with less than 12 yr of schooling, compared with adults who had attended college. The high rate of acquisition of H. pylori infection in Saudia Arabia emphasizes that studies of H. pylori-disease associations must consider the baseline prevalence of H. pylori infection in that population.
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PMID:Prevalence of Helicobacter (formerly Campylobacter) pylori infection in Saudia Arabia, and comparison of those with and without upper gastrointestinal symptoms. 237 21

We investigated the distribution and prevalence of Campylobacter pylori in the stomach and duodenum. In this study, 500 biopsy specimens were obtained from 245 patients. In each case, biopsy specimens were taken from more than 2 sites. C. pylori was detected by culture, urease test and acridine-orange stain. C. pylori was not detected on the intestinal metaplasia, gastric cancer tissue and duodenal mucosa without gastric metaplasia. In 21% of cases, C. pylori was detected in only one site. Because of the patchy distribution of C. pylori, more than 2 biopsy specimens from different sites were needed to avoid sampling error. Detection rate of C. pylori was almost equal in antrum, angle and body as well as in male and female. H2 receptor antagonists did not affect the detection rate of C. pylori. According to the endoscopic diagnosis of the biopsied site, C. pylori was detected in 87% of gastric ulcer, 60% of duodenal ulcer (duodenal mucosa with gastric metaplasia), 73% of chronic gastritis and 62% of endoscopically normal gastric mucosa.
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PMID:[Distribution and prevalence of Campylobacter pylori in the stomach]. 257 39

To investigate the prevalence of Campylobacter pylori (CP) and its association with histological inflammatory grading and intestinal metaplasia, biopsies were carried out in 388 patients with gastro-duodenal diseases from 2 sites in the stomach (body and antrum). In each case, 3 biopsy specimens were taken from each site for culture, acridine orange stain and urease test. CP was detected in 55% of 22 endoscopically normal patients, in 47% of 17 gastric cancer patients, in 73% of 205 gastritis patients in 91% of 99 gastric ulcer patients and in 100% of 45 duodenal ulcer patients. In gastric ulcer and duodenal ulcer patients, CP detection rate was significantly higher than in endoscopically normal patients (p less than 0.01). There was no difference in CP detection rate irrespective of ulcer stage (active, healing or scar). According to the histological gradings of inflammation (Warren's criteria), CP was detected in only 3% in grade 0-I, 20% in grade II and 83% in grade III. It was found that a close association between CP and histological gastritis with polymorphonuclear leukocytes infiltration exists (p less than 0.001). In a few cases, CP was found even in the areas of intestinal metaplasia. But the number of CP in the areas of intestinal metaplasia were fewer than in the areas of surrounding inflamed gastric mucosa. In most cases, CP was not seen in the areas of intestinal metaplasia, but was found in the areas of surrounding inflamed gastric mucosa in the same biopsy specimen.
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PMID:[Campylobacter pylori in gastro-duodenal diseases, with special reference to endoscopic diagnosis, histological inflammatory grading, and intestinal metaplasia]. 279 52

Campylobacter pylori causes type B gastritis and C. pylori infection has been associated with duodenal ulcer, gastric ulcer, non-ulcer dyspepsia, and gastric cancer. Although we have been able to culture C. pylori for only about 5 years, what we now know about this organism can explain many mysteries surrounding peptic ulcer disease. Whenever one investigates a population of ulcer patients for the presence of any accepted potentially important pathogenetic factors, one finds that the population of patients with duodenal ulcer disease differs (statistically) from those without duodenal ulcer disease, but that to a large degree they also overlap. None of the traditional factors can be considered essential and characteristic of chronic duodenal ulcer. The exception is the presence of a C. pylori infection, the presence of which is almost invariable. Several properties of C. pylori have been identified that might be virulence factors, including (a) provoking a marked acute and chronic inflammatory response, (b) rapid motility through gastric mucus, (c) urease activity, (d) a fibrillar adhesin(s), (e) several putative exotoxins, and (f) microinvasion. We can now add to the old dictum "no acid-no ulcer," "no C. pylori-no ulcer" at least as far as chronic duodenal ulcer disease in adults is concerned.
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PMID:Campylobacter pylori. The organism and its clinical relevance. 280 38


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