Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.5.1.5 (urease)
7,257 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Helicobacter pylori infection and adenomatous polyposis coli (Apc) gene mutations have been linked to gastric cancer in humans, but possible synergistic interaction(s) between these risk factors have not been examined. Fourteen C57BL/6 wild-type and 14 Apc1638 heterozygous mice were inoculated with Helicobacter felis at 6 weeks of age and compared at various time points with a similar number of uninfected control mice of the same genotype. Both infected and uninfected Apc1638 mice had a limited incidence of atypical proliferation foci in the mucosa of the antrum and pyloric junction at 4.5 and 6 months of age, whereas polyps of the antrum and pylorus were present in all mice, regardless of infection status, at 7.5 months. In contrast, no altered gastric mucosal foci were observed in control or infected C57BL/6 mice at any time point. Interestingly, the infected Apc1638 mice had less epithelial proliferation and inflammation in the body of the stomach, lower anti-H. felis serum IgG antibody responses (although both the wild-type and Apc mutant mice had a Th1-like immune response, based on a predominantly IgG2a immunoglobulin response), and higher bacteria and urease scores than did infected wild-type C57BL/6 mice. In conclusion, the Apc1638 truncating mutation leads to gastric dysplasia and polyposis of the antrum and pyloric junction, but H. felis infection of the Apc mutant mouse does not lead to an increased rate of gastric neoplasia. In addition, our data suggest this Apc mutation may actually lead to decreased immune, inflammatory, and gastric hyperplastic responses to Helicobacter infection, suggesting the possibility of a novel role for this tumor suppressor gene in the immune and local tissue responses to gastric bacterial infection.
Cancer Res 1997 Sep 15
PMID:Mice carrying a truncated Apc gene have diminished gastric epithelial proliferation, gastric inflammation, and humoral immunity in response to Helicobacter felis infection. 930 81

The role of Helicobacter pylori in gastric carcinogenesis is a subject of an increasing interest. In this report we describe a prospective study on the resected stomachs to establish the prevalence of H. pylori in different types of gastric carcinoma. The material consisted of 62 consecutive patients operated on stomach adenocarcinomas Fifty six percent of the patients were intestinal type, 34%--diffuse type and 10%--mixed type. The presence of H. pylori was studied in specimens from surgically removed stomachs. The conformation of the bacterial infection was done by means of rapid urease test, microbiological culture, Warthin-Starry and immunohistochemical staining. The overall prevalence of H. pylori infection was 69% (43/62). There was a statistically significant difference in the infection rates between the types of carcinoma--75% in the intestinal type and 62% in the diffuse type. The most sensitive was immunohistochemical staining. The bacterial colonies were cumulated far from the tumor tissue. In cardiac cancer the most intense of infection was an antrum and lower part of gastric body. In opposite; in antrum and pylorus cancer the scope of colonisation increased in fundus and subcardiac region with statistical signification. We could not detect H. pylori in the tumor tissue itself as in the normal mucosa of the stomach. In gastric antrum the most intense colonisation was detected on mucosal atrophy, but in the upper part of the stomach--on the mucosal metaplasia.
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PMID:Topography of Helicobacter pylori infection in gastric cancer patients. 944 64

To evaluate if the infection with strains of cytotoxin-associated gene A (CagA)-positive Helicobacter pylori is associated with either peptic ulcer and gastric atrophy or intestinal metaplasia in the elderly, we studied 71 H. pylori-positive patients older than 62 years old (34 men, 37 women; mean age, 77.5 years; range, 62-89 years) affected with gastric ulcer (GU) (n = 10), duodenal ulcer (DU) n = 22), or chronic gastritis (CG) (n = 39). H. pylori infection was documented by means of gastric histology, rapid urease test, and polymerase chain reaction (PCR) assay performed on gastric biopsies using two sets of primers: one for the ureC gene specific for H. pylori, and the second specific for the CagA gene. H. pylori-CagA positivity was significantly more common in patients with GU (9 of 10, 90%) than with DU (11 of 22, 50%; p < 0.05) or CG (17 of 39, 43.5%; p = 0.01). Gastric atrophy and intestinal metaplasia were significantly more common in CagA-positive patients than in CagA-negative patients (gastric atrophy: 40.54% vs 11.76, p = 0.007; intestinal metaplasia: 40.54% vs 14.70%, p = 0.01). No difference in prevalence of gastric atrophy and intestinal metaplasia was found in patients divided according to pathology (GU, DU, or CG). Logistic regression demonstrated that gastric atrophy and intestinal metaplasia were independent factors significantly associated with CagA-positivity (gastric atrophy: odds ratio = 4.53, 95% confidence interval 1.25-16.4; intestinal metaplasia: odds ratio = 3.44, 95% confidence interval 1.01-11.7). Our findings help to confirm the hypothesis that an infection with CagA-positive H. pylori strains may be catalytic in inducing gastric changes which can evolve into malignancies.
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PMID:Cytotoxin-associated gene A-positive Helicobacter pylori infection in the elderly. Association with gastric atrophy and intestinal metaplasia. 949 57

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.
Jpn J Cancer Res 1998 Jun
PMID:Association of Helicobacter pylori infection with gastric adenocarcinoma. 970 56

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

The detection of HP infection by means of non invasive methods such as breath test and urease test, which are adopted alternatively to histological examination, can delay the diagnosis of early lymphomas. On the other hand the proved regression of gastric low grade Malt lymphomas after a successful HP eradication strongly suggests the need for early diagnosis. The aim of this study was to report the results of our experience with regard to clinical, endoscopic, histopathologic, and immunohistochemical features of gastric MALT lymphomas. We studied twenty-seven consecutive cases of gastric Malt lymphoma. HP presence in gastric mucosa was detected in all cases but endoscopy only in 40.7% of cases giving a diagnosis of suspected malignancy. In conclusion, it is very important to sample gastric mucosa in HP positive patients because the histological examination represents the most effective tool to detect lesions at the earliest and curable stage.
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PMID:Gastric Malt lymphoma: a clinicopathological study. 985 95

Helicobacter pylori is the most common bacterial pathogen world-wide and has been identified in all countries. As long-term infection with H. pylori could potentially lead to duodenal or gastric ulcer disease, asymptomatic chronic gastritis, chronic dyspepsia, or gastric malignancy, including both adenocarcinoma and B-cell lymphoma, a large number of different treatment regimens aimed at eradicating H. pylori has been evaluated and reported. Despite numerous H. pylori treatment studies the optimum regimen for its eradication remains unclear. A treatment regimen, which is effective, safe and inexpensive could be used widespread and reduce the risks of the long-term complications of infection. In this study we compared the efficacy, side effects and cost-effectiveness of 12 different therapy regimens for H. pylori eradication by using meta-analysis methodology. 486 patients (256 male, 230 female; mean age 40.8 years) with H. pylori associated duodenal ulcer (n = 140), gastritis (n = 254), gastroduodenitis (n = 92) were treated with 12 different therapy-regimens. Endoscopy was performed at baseline and 6 weeks after discontinuation of eradication therapy. H. pylori status was assessed by urease test and histology. The therapy with a H2-receptor antagonist is less effective than the triple therapies with omeprazole or lansoprazole. Bismuth-based triple therapies have a mean overall eradication rate of 68%, but are limited by frequent side effects causing poor drug compliance.
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PMID:[Meta-analysis of determining the pathogen eradicating efficacy of various therapeutic regimens in Helicobacter pylori infection]. 1002 50

Helicobacter (Campylobacter) pylori infection has emerged as a major cause of gastritis, peptic ulcers, and gastric malignancies. Not all patients with H. pylori infection require treatment; however, for those with ulcer disease (particularly those with bleeding), antibiotic therapy can be curative. To confirm infection (or its eradication), use the rapid urease assay, serologic examination or, when available, the urea breath test. Treatment options include triple therapy (with bismuth subsalicylate, metronidazole, and either tetracycline or amoxicillin) and dual therapy (with omeprazole and either amoxicillin or clarithromycin). For patients with an active ulcer, follow antibiotic therapy with ranitidine or omeprazole.
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PMID:H. pylori infection and GI disease: what critical care physicians need to know. Who should be tested for H. pylori? When is treatment needed? 1015 Apr 1

Several species of Helicobacter colonize the hepatobiliary tract of animals and cause hepatobiliary diseases. The aim of this study is to investigate Helicobacter found in the biliary tract diseases of humans. Thirty-two bile samples (15 from bile duct cancer, 6 from pancreatic head cancer, and 11 from intrahepatic duct stone) were obtained by percutaneous transhepatic biliary drainage. Polymerase chain reaction analysis using Helicobacter specific urease A gene and 16S rRNA primers, bile pH measurement, and Helicobacter culture were performed. Helicobacter DNA was detected in 37.5%, and 31.3% by PCR with ureA gene, and 16S rRNA, respectively. The bile pH was not related to the presence of Helicobacter. The cultures were not successful. In conclusion, Helicobacter can be detected in the bile of patients with bile duct diseases. The possibility of pathogenesis of biliary tract diseases in humans by these organisms will be further investigated.
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PMID:Detection of Helicobacter DNA in bile from bile duct diseases. 1033 65

A high-salt diet in humans and experimental animals is known to cause gastritis, has been associated with a high risk of atrophic gastritis, and is considered a gastric tumor promoter. In laboratory rodents, salt is known to cause gastritis, and when coadministered, it promotes the carcinogenic effects of known gastric carcinogens. Because Helicobacter pylori has been associated with a progression from gastritis to gastric cancer, we designed a study to determine whether excessive dietary NaCl would have an effect on colonization and gastritis in the mouse model of H. pylori infection. Seventy-two, 8-week-old female C57BL/6 mice were infected with H. pylori strain Sydney, and 36 control mice were dosed with vehicle only. One-half of the infected and control mice were fed a high-salt diet (7.5% versus 0.25%) for 2 weeks prior to dosing and throughout the entire experiment. Twelve infected and 6 control animals from the high-salt and normal diet groups were euthanized at 4, 8, and 16 weeks. At 8 and 16 weeks postinfection (WPI), the colony-forming units per gram of tissue were significantly higher (P < 0.05) in the corpus and antrum of animals in the high-salt diet group compared with those on the normal diet. Quantitative urease was significantly higher (P < 0.05) at 4 and 8 WPI in the corpus and antrum of animals on the high-salt diet when compared with controls. At 16 WPI, mice in both the normal and the high-salt diet groups developed moderate to marked atrophic gastritis of the corpus in response to H. pylori infection. However, the gastric pits of the corpus mucosa in mice on the high-salt diet were elongated and colonized by H. pylori more frequently than those in mice on the normal diet. The high-salt diet was also associated with a significant increase in proliferation in the proximal corpus and antrum and a multifocal reduction in parietal cell numbers in the proximal corpus, resulting in the elongation of gastric pits. We conclude that excessive NaCl intake enhances H. pylori colonization in mice and in humans and that chronic salt intake may exacerbate gastritis by increasing H. pylori colonization. Furthermore, elevated salt intake may potentiate H. pylori-associated carcinogenesis by inducing proliferation, pit cell hyperplasia, and glandular atrophy.
Cancer Res 1999 Oct 01
PMID:High-salt diet induces gastric epithelial hyperplasia and parietal cell loss, and enhances Helicobacter pylori colonization in C57BL/6 mice. 1051 91


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