Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:6.3.4.6 (urease)
 7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There seems to be a worldwide geographic variation in the prevalence of peptic ulcer disease, although there are few reliable population based studies. This study aimed to determine the prevalence of peptic ulcer disease in a community in southern India and to evaluate the relationship between dyspeptic symptoms, Helicobacter pylori infection, gastritis, and peptic ulcer disease. A sample population was selected randomly from a rural monastic settlement in southern India. Subjects were interviewed using a standardised symptom and demography questionnaire then underwent upper endoscopy and antral biopsy for histology and CLO rapid urease test. Altogether 197 subjects from a population of 1499 (13.1%) were studied. All were male monks and ethnically Tibetan. The median age was 28 years (range: 21-81). None smoked or took NSAIDs. The six month period prevalence of dyspeptic symptoms was 68.5%. Current symptoms were present in 58.9% of subjects. Dyspepsia was more common in subjects aged 40 years or younger (p < 0.0001). H pylori was detected in 77.2% subjects. There was no association between dyspepsia and the presence of H pylori or histological gastritis, although there was a strong correlation between symptoms and ulcer (p < 0.003). The point prevalence of active peptic ulcer was 6.6% (13/197). All ulcers detected were either prepyloric or pyloroduodenal in location. A further 6.6% of subjects had definite evidence of scarring or deformity indicative of ulceration in the past. Subjects with past or present ulcers comprised 17.8% of dyspeptic subjects. H pylori was present in all subjects with active ulcers and in 12/13 of those with scarring. Dyspepsia, H pylori infection, gastritis, and peptic ulcer are all more common in this population than in those from developed countries. Ulcer disease, however, accounts for only a small proportion of subjects with symptoms and neither H pylori infection nor gastritis are significantly associated with the presence of dyspepsia.
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PMID:Dyspepsia, Helicobacter pylori, and peptic ulcer in a randomly selected population in India. 145 68

To determine whether omeprazole eradicates Helicobacter pylori infection of the gastric antrum, six adolescents and one adult with H. pylori colonization of the antrum were entered into a clinical, open trial of medical therapy. Histologic evidence of antral gastritis and three complementary methods to document H. pylori colonization of the stomach (silver stain, urease testing, and culture of antrum) were obtained before and after an 8-week course of omeprazole. In vitro susceptibility to omeprazole and restriction endonuclease analysis were performed on H. pylori isolates obtained from patients before and after omeprazole therapy. Each of the seven patients treated with omeprazole had continued active inflammation in the antrum and one or more features indicative of persisting H. pylori colonization. Minimum inhibitory concentrations and DNA fingerprints of H. pylori isolated after therapy were identical to those of the pre-treatment bacterial isolates in each of the four subjects examined. We conclude that omeprazole therapy alone did not eradicate H. pylori infection of the human antrum. Continued bacterial colonization was not related to either acquired bacterial resistance to the drug or reinfection of the stomach with a different H. pylori strain.
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PMID:Omeprazole therapy for Helicobacter pylori infection. 147 17

This prospective study aimed to determine the prevalence of Helicobacter pylori infection in relation to the occurrence and severity of NSAIDs induced gastropathy. A total of 111 patients were studied-66 were taking NSAIDs and 45 were control patients. All patients underwent endoscopy during which antral biopsy specimens were taken to determine H pylori status (Gram and Giemsa staining, urease test, and cultures). The NSAID group comprised: group I, patients without mucosal damage (n = 28); group II, patients with gastropathy (n = 26); and group III, patients with bleeding associated with NSAID induced gastropathy (n = 12). Control patients had neither dyspeptic symptoms nor endoscopic lesions. There were no differences in age, sex ratio, or presence of H pylori (26% v 24%) between the NSAID and the control groups. Among patients taking NSAIDs, H pylori infection was more frequently (p < 0.02) diagnosed in those who presented with gastropathy (groups II and III: 37%) than in those without lesions (group I: 11%). The frequency of H pylori infection increased significantly with the severity of gastropathy (group I = 11%; group II = 31%; group III = 50%; p < 0.03). H pylori infection was associated with chronic active gastritis (group I = 21%; group II = 35%; group III = 67%; p < 0.05). These data suggest that H pylori may be a risk factor of NSAID induced gastropathy.
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PMID:Helicobacter pylori: a risk and severity factor of non-steroidal anti-inflammatory drug induced gastropathy. 148 60

The urease of Helicobacter pylori is suspected to play a role in the pathogenesis of gastritis. Although all clinical isolates of H. pylori are urease positive (U+), we have selected and characterized several spontaneously arising urease-negative (U-) variants from wild-type strain 60190. Urease-negative variants were identified by growth in medium containing 60 mM urea and arose at a frequency of 10(-5) to 10(-6). The urease activity of the wild-type strain inhibited growth of this strain in the presence of 60 mM urea. U- variants retained the U- phenotype for more than 100 passages on medium with or without urea. The urease activities of the original U+ and derived U- cells were 9.55 to 16.7 and 0.01 to 0.17 U/mg of protein, respectively. Colonial growth and other biochemical characteristics were identical for the strains. U- variants showed three classes of whole-cell sodium dodecyl sulfate-polyacrylamide gel electrophoresis profiles: (i) identical to U+; (ii) change in the migration of the 61-kDa urease subunit; and (iii) lack of 61- and 30-kDa subunits. These differences were confirmed by immunoblotting and by protein separation using fast protein liquid chromatography. The U+ strain but not U- variants tolerated exposure to pH 4.0 for 60 min in the presence of urea. Supernatants of the U+ strain and U- variants contained vacuolating cytotoxin activity for HeLa cells in similar titers. By enzyme-linked immunosorbent assay, human serum samples recognized water extract from the U+ strain significantly better than extract from a U- variant lacking urease subunits. In conclusion, this study demonstrates that U- H. pylori variants may arise spontaneously, that urease activity enhances survival at acid pH, and that urease and cytotoxin activities are disparate phenotypes.
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PMID:Characteristics of Helicobacter pylori variants selected for urease deficiency. 150 Jan 74

Helicobacter pylori is associated with chronic type B gastritis. Diagnosis can be made on gastric biopsy specimens and noninvasively using [13C]- or [14C]urea breath tests. Both breath tests require meticulous breath collection, and false positive results are possible from urease producing oral-pharyngeal flora. We used [11C]urea, a positron-emitting radionuclide allowing dynamic imaging, to measure metabolism of urea in the stomach of biopsy documented H. pylori-positive patients. [11C]urea was synthesized from 11CO2 produced using a Van de Graaff accelerator and administered with [99mTc]DTPA to control for loss of radioactivity via gastric emptying. Images were obtained externally by gamma camera every minute and 11CO2 was monitored in the breath continuously for 30 min. An H. pylori-positive patient exhibited a 99mTc/11C activity ratio of 2:1 in the stomach 10-20 min following administration, compared to a 1:1 ratio in a negative control, indicating metabolism of urea to 11CO2 with subsequent diffusion of 11C activity out of the stomach. The 11C activity in the breath peaked at 10-20 min in the H. pylori-positive patients. The short half-life of carbon-11 (20.4 min) alleviates radiation safety concerns and results in low absorbed radiation doses to patients.
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PMID:Noninvasive detection of Helicobacter pylori colonization in stomach using [11C]urea. 155 56

A prospective study was conducted to determine the frequency of occurrence of Helicobacter pylori infection in outpatients presenting with upper gastro intestinal symptoms to Arba Minch Hospital over a one year period. Four hundred and forty four patient, 309 males and 135 females, underwent upper gastro intestinal fiberoptic endoscopy between March 1989 and April 1990. The age range was 14 to 75 years (mean = 35). All 444 patients were examined and tested for infection. Sixty per cent had abnormal endoscopy results. The major endoscopic findings were gastritis in 23% and peptic ulcer disease in 20% of the patients. To identify H. pylori infection, 2 biopsy specimens were taken from the greater curve of the gastric antral mucosa of all patients. The specimens were examined using the urease diagnostic test and Loeffler Methylene Blue stain. Infection was considered present when either of the tests were positive. Infection by H. pylori was found in 324 patients (73%). Among the 173 patients without endoscopic findings, 63% had infection. Of 271 patients with abnormal endoscopic findings, 79% were infected. The results of this study show that H. pylori infection is a common finding in patients with upper gastrointestinal symptoms in Ethiopia. There is a higher prevalence of infection among patients with endoscopic findings. Thus the management of patients with upper gastro-intestinal symptoms in Ethiopia should take H. pylori infection into consideration.
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PMID:Helicobacter pylori infection in patients with upper gastrointestinal symptoms in Arba Minch Hospital: southwestern Ethiopia. 156 64

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

Twenty-five Helicobacter pylori positive and 25 H. pylori negative subjects as defined by culture and phase contrast microscopy of antral biopsy specimens obtained from routine upper endoscopy were studied. Antral biopsies were examined by rapid urease test, phase contrast microscopy, culture and histology. Venous blood was tested for H. pylori specific IgG antibodies by an ELISA technique. Within 7 days of endoscopy the patients also had a [14C]-urea breath test. The sensitivity and specificity of the rapid urease test was 92%, the breath test 96% and 100%, histopathology 96% and 91% and serology 96% and 88%, respectively. The [14C]-urea breath test performed over 1 h with sampling of subjects at 0, 0.5 and 1 h was an accurate and reliable method. Results expressed as counts per minute of the expired 14CO2 proved to be a simple method of assessing H. pylori status. A significant correlation between severity of histological antral gastritis and the amount of 14CO2 expired was observed. This study has shown that the non-invasive 14C-urea breath test and serology are highly sensitive and specific for the diagnosis of H. pylori infection.
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PMID:A comparison of diagnostic tests to determine Helicobacter pylori infection. 157 5

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

The variation in the healing and the relapse rates of peptic ulcer disease has led to the search for other factors in the pathogensis of peptic ulcer disease. Helicobacter pylori is believed to be responsible for these different patterns of healing. The results of a study to detect Helicobacter pylori in Sri Lankan patients having duodenal ulcer, gastric ulcer, gastritis and non-ulcer dyspepsia are presented in this paper. The method employed was the urease test which detects the urease enzyme of H. pylori in gastric mucosal biopsies taken during upper gastrointestinal endoscopy. There is a high incidence in those with gastritis and duodenitis.
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PMID:Helicobacter pylori and peptic ulcer disease in Sri Lanka. 158 90


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