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

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

As shown by means of temperature-perturbation differential spectrophotometry blood serum immunoglobulins G from patients with gastric cancer and with some other tumors were more resistant to 2 M urea as compared with the immunoglobulins from healthy volunteers and patients with gastric ulcerous disease. The resistance of IgG conformation was altered in the course of gastric cancer treatment.
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PMID:[Stability of serum immunoglobulin conformation in various tumors]. 175 Feb 1

We collected clinical, laboratory and endoscopic data prospectively in patients presenting with acute non-variceal upper gastrointestinal bleeding admitted to the care of one surgical team. During a 30-month period 52 patients were subsequently proven to have gastric adenocarcinoma; 30 patients underwent elective operation, and emergency surgery for bleeding was performed on 14 occasions. There were 13 hospital deaths (25%), 13.5% at 30 days. Emergency surgery was associated with a higher mortality rate (42.9%) than elective procedures (13.3%) (P less than 0.03). Factors associated with a poor prognosis were active haemorrhage at initial endoscopy, an admission blood urea nitrogen greater than 16 mmol/l, preoperative transfusion greater than 4 units, total transfusion greater than or equal to 9 units and a lowest recorded haemoglobulin during hospitalization of less than 7.5 g/dl. The unacceptably high mortality rate associated with surgery for continued haemorrhage or rebleeding episodes suggest that earlier elective operative intervention be advocated in patients presenting with acute bleeding and in whom gastric cancer is visualized. This is recommended particularly if the initial bleeding episode is severe, or active haemorrhage is visualized during initial endoscopy.
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PMID:Risk factors for mortality in patients with gastric adenocarcinoma presenting with acute haemorrhage. 204 79

Results of five non-specific reactions (ceruloplasmin assay, Ehrlich's reagent colorimetry, heat-resisting reaction of serum and determination of indole and neutral sulphide in urea) for the diagnosis of gastric carcinoma were calculated by the use of multiple-factor analysis. The positive rates in 284 cases of gastric carcinoma (including 8 early lesions), 306 healthy donors and 1018 cases of benign gastric diseases were 78.2% (62.5% for the early gastric cancers), 0.7% and 15.7%, respectively. The results showed that these tests are valuable for the screening in a high incidence area of gastric cancer or as a supplementary diagnostic means of gastric carcinoma in clinical practice.
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PMID:[Diagnosis of gastric carcinoma with a group of biochemical tests]. 408 15

Helicobacter pylori (Hp) has been associated to gastritis, peptic ulcer, gastric cancer, and other gastrointestinal disorders. The 14C-urea breath test (UBT) has been proposed as a simple and noninvasive method for its detection, and has recently been implemented in our institution. To optimize our resources, we performed a sensitivity analysis to determine the minimal sampling and duration of testing required, and to establish objective criteria for its interpretation. With this purpose, endoscopy, antral biopsy and UBT were performed in 104 dyspeptic patients. For the UBT, a basal breath sample was taken before the administration of 10 microCi of 14C-urea and followed by sequential breath sampling at 5, 15, 30 and 60 minutes. Considering histologic findings as the gold standard, receiver operating characteristic (ROC) curves were constructed for the following three 14CO2 excretion strategies: excretion by sample, maximum excretion, and cumulative excretion. Hp was detected in 74 (71%) of the patients, and its presence coincided with significantly higher 14CO2 excretion than in the Hp negative (p < 0.001). The three excretion strategies were comparable in terms of diagnostic accuracy, but the most efficient results were given by the 15 minute sample. With a cut-off point of > or = 1.7%, the sensitivity and specificity of this sample was > or = 83%, the positive and negative predictive values were 93% and 68%, and the accuracy was 84%. We conclude that UBT can be completed with a single breath sampling at 15 min, and its results objectively interpreted as positive if the 14CO2 excretion is > or = 1.7%.
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PMID:[Optimization of the tagged urea test for the detection of H. pylori in patients with dyspepsia]. 761 Feb 79

We apply the thermal perturbation difference spectroscopy to demonstrate that immunoglobulins G (IgG) isolated from blood serum of a patient with stomach cancer are more stable to the influence of 12% urea than IgG of a healthy donor. IgG at the same pathology have greater tendency to aggregation than IgG at norm according to the laser correlation spectroscopy data.
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PMID:[Aggregation of human immunoglobulins under normal conditions and in malignant stomach tumor]. 770 76

Recently pepsinogens have been considered to be effective markers of terminal differentiation of stomach mucosa, and also good markers of preneoplastic and neoplastic changes of the stomach mucosa. Not a few studies concerning polymorphisms of pepsinogen A and C genes have been reported, however, as far as the authors are aware, no study was performed as to the relation between polymorphisms and serum pepsinogen I and II levels. Polymorphisms of the pepsinogen C (PGC) gene were identified by PCR, which amplifies DNA in the region within the intron between exon 7 and exon 8, and 6% polyacrylamide gel (no urea) electrophoresis. Six alleles were observed in the Japanese population. Frequencies for these alleles in 221 unrelated Japanese individuals were 0.077, 0.036, 0.328, 0.240, 0.009 and 0.310, respectively. The association between the PGC genotype and serum pepsinogen was investigated. A higher serum pepsinogen II level was observed in individuals homozygous for allele 6 than in those with other genotypes. This result indicates that careful attention should be paid to the genetic background of serum pepsinogen in screening of stomach cancer by this method.
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PMID:[Effects of pepsinogen C gene polymorphisms on serum pepsinogen I and serum pepsinogen II levels]. 772 83

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

Recently many reports have shown a strong association between Helicobacter pylori infection in the stomach and recurrent peptic ulcer. Moreover, prospective cohort serological studies showed that H. pylori infected individuals have significantly increased rate of gastric cancer in the USA. H. pylori is a gram-negative spiral organism which has urease activity and produces ammonia and CO2 from urea, and nestles in the gastric pits and overlaying mucus gel layer. Many diagnostic methods of H. pylori infection are available; ie bacterial culture, 13C-urea breath test, histology, serum IgG antibody against H. pylori. We developed a new method, ie tissue IgA antibody against H. pylori and detection of H. pylori DNA in the gastric juice by PCR method. Triple therapies with metronidazole, bismuth compounds, and amoxicillin or tetracyclin are difficult to use in Japan because of their sever side effects. Thus, new methods with proton pump inhibitor (PPI) and amoxicillin have been introduced. We treated 14 patients of whom were H. pylori positive-active peptic ulcer with 30 mg/day of lansoprazole, a new PPI, plus 1,500 mg/day of amoxicillin for 2 weeks and 8 (57%) patients were eradicated. Gastric carcinogenesis are multi-steps and multifactorials process. Hypothetical sequence of intestinal type of gastric cancer is that superficial gastritis-->atrophic gastritis-->intestinal metaplasia-->dysplasia-->gastric cancer and H. pylori infection may play a role in the early stage of the sequence. We examined mucosal IgA antibody against H. pylori in chronic gastritis and intestinal metaplasia detected by the Tes-Tape method in 25 resected specimens after gastrectomy for gastric cancer. Positivity rates of tissue H. pylori IgA antibody were lower in the mucosa of intestinal metaplasia than in non-metaplastic gastric mucosa and were negative in carcinoma. Causal relationship between H. pylori infection and gastric cancer is not proven and factors other than H. pylori infection are also important in the gastric carcinogenesis. Finally we introduce 2 reports: (1) NIH Consensus Conference: Helicobacter pylori in peptic ulcer disease (JAMA. 1994; 272: 65-69). The consensus panel concluded that 1. ulcer patients with H. pylori infection require treatment with antimicrobial agents in addition to antisecretory drugs whether on first presentation with the illness or on recurrence; 2. the value of treating nonulcerative dyspepsia patients with H. pylori infection remains to be determined; and 3. the interesting relationship between H. pylori infection and gastric cancer requires further exploration. (2) World Health Organization: Working Group Meeting (Reported in World Congress of Gastroenterology, Los Angeles, 1994). H. pylori plays a causal role in the chain of events leading to cancer of the stomach. Group I: definite carcinogen.
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PMID:[Helicobacter pylori in peptic ulcer and gastric cancer]. 785 88

Helicobacter pylori is part of a genus of specialized bacteria that have adapted to the ecological niche provided by gastric mucus. H. pylori has exploited the human niche, while further species of Helicobacter have inhabited the gastric mucosa of other animals. The preferred habitat of H. pylori is the gastric antrum. In humans with normal gastric function, the organism is mainly restricted to the antral surface, where a number of specialized traits allow it to flourish, while causing minimal harm to its host. These include a characteristic motility that allows it to swim rapidly through viscous mucus, and the ability to manufacture large amounts of the enzyme urease. This enzyme breaks down endogenous urea to form ammonia, which protects the bacterium from gastric acidity. Specific adhesions bind a number of the bacteria to the gastric surface, some swim freely in the mucus, and others possibly endocytose into the epithelial cells. It is probably these inaccessible colonization sites that make the organism so difficult to eradicate. In some patients, the normally harmless balance between host and bacterium is disturbed, resulting in peptic ulceration. Modifications to the mucus or epithelial surface in the proximal duodenum, towards the gastric phenotype, make the tissue more susceptible to H. pylori infection of the duodenum by spread of organisms from the antrum. Gastric acid output becomes further increased and the duodenal mucosa is rendered more susceptible to acid attack, leading to peptic ulceration. In other situations, the level of inflammation is enhanced and immunopathology results, followed in the longer term in some cases by atrophy and gastric cancer.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The microbiology and epidemiology of Helicobacter pylori infection. 804 19


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