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)

Helicobacter pylori is a microaerophilic, Gram-negative, spiral rod, the role of which in different gastric diseases has been investigated worldwide since the beginning of the 1980s. H. pylori has been shown to be the causative agent in active chronic gastritis, and it is regularly found in patients endoscopied for duodenal ulcer. The bacterium is also frequently isolated from persons with gastric ulcer, gastric carcinoma and non-ulcer dyspepsia. Apart from cultivation of the bacterium, other diagnostic procedures include various staining methods and urease tests of gastric biopsy samples. The application of non-invasive diagnostic methods, serology and urea breath tests, is rapidly increasing. H. pylori is susceptible to several antimicrobials in vitro, but eradication of the bacterium from the gastric mucosa is not always achieved. The best results until now have been obtained with the combined use of bismuth salts and two antibiotics. In active chronic gastritis and duodenal ulcer patients, eradication of the bacteria has resulted in healing of the disease with permanent decrease of circulating antibodies and negative urease tests. H. pylori has been found worldwide and the infection shows an age-dependent increase. Man, apparently, is the reservoir of the bacterium, but the exact mechanisms of interhuman transmission are still not defined.
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PMID:Helicobacter pylori and associated gastroduodenal diseases. Review article. 185 43

Diagnostic accuracy of 5 tests viz., endoscopy, rapid urease, 24 hours urease, culture and histology, were evaluated in the detection of Helicobacter pylori (H. pylori) infection in 50 patients undergoing upper G.I. endoscopy. Endoscopic evidence of gastritis to predict H. pylori infection was 50% specific and 46% sensitive. Rapid and 24 hours urease test and culture were 100% specific when compared with histology and their sensitivity was 71%, 62% and 21% respectively. Of the three 100% specific tests, rapid urease test yields results within 15 minutes; therefore this test being easy, rapid and sensitive should be used for screening of H. pylori infection; followed by histology for further confirmation.
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PMID:Can diagnosis of Helicobacter pylori be rapid and yet sensitive? 186 52

Helicobacter mustelae is a urease-rich bacterium associated with gastritis in ferrets. The ureases of H. mustelae and Helicobacter pylori, a bacterium implicated in human gastritis, share many characteristics. Helicobacter sp. ureases appear to be unique among bacterial enzymes in exhibiting submillimolar Km values and in being composed of two subunits.
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PMID:Purification and characterization of Helicobacter mustelae urease. 187 50

Most patients with chronic duodenal ulcer (DU) craters have gastritis associated with Helicobacter pylori (HP), now thought to be the major cause of DU. A smaller proportion of DU patients have no detectable HP. In this study, we examined the frequency and causes of HP-negative duodenal ulcers. In 302 consecutive patients with endoscopic diagnosis of duodenal ulcer, 284 (94%) were found to have associated HP gastritis, whereas 18 (6%) were HP-negative on histology, culture, and urease test. The largest subgroup of HP-negative patients (8/18) was made up of those who had been taking nonsteroidal antiinflammatory drugs (NSAIDs), followed closely (4/18) by patients with recent intake of antibiotics. Causes of DU in the remaining subgroups included two patients with duodenal Crohn's disease, two with Gastrospirillum hominis infection, one with penetrating carcinoma of the pancreas and one with no detectable cause. We conclude that, although the most common causal factor of duodenal ulcer is HP, some 6% of DU's will be HP-negative, signaling unusual etiology. It is now important to identify the cause of duodenal ulcer so as to initiate appropriate therapy.
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PMID:Helicobacter pylori-negative duodenal ulcer. 188 93

Helicobacter pylori has recently been recognized as a gastric pathogen in humans. Experimental oral inoculation of gnotobiotic piglets with this organism results in gastritis that exhibits many features of the corresponding disease in humans. In piglets the organism is restricted to the gastric microenvironment and persists in that location despite prompt humoral and cellular responses to antigens of H. pylori. The gnotobiotic piglet model is useful for delineation of the role of suspected bacterial virulence factors (i.e., motility and urease production) in gastric colonization and for preclinical determination of the efficacy of various antimicrobial substances.
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PMID:Gastritis induced by Helicobacter pylori in gnotobiotic piglets. 192 8

Two-hundred and ten consecutive patients undergoing routine gastroscopy were additionally investigated for evidence of Campylobacter pylori (C.p.). 106 patients were positive in one or more tests: 99.1% using a rapid urease detecting test (CLO-test), 80.2% histology, 78.3% cytology and 60% culture. We found no difference between the CLO-test results from biopsies taken from different parts of the stomach in individual patients. C.p. was found in 100% of patients with significant chronic antral gastritis, 67.7% with gastric ulcers, 65% with duodenal ulcers and in 12.1% of normal individuals. The C.p. infection was apparently eliminated in 50% of cases treated with bismuth subsalicylate (BSS) for four weeks. The combination of BSS with amoxicillin, tinidazole or an H2-receptor antagonist offered no advantage over BSS alone. Treatment with BSS led to improvement in symptoms and histological findings including healing of ulcers in patients with or without persistent C.p. infection. The recurrence of C.p. infection after apparently successful treatment was, however, 75% in 4 weeks. In conclusion, C.p. infection correlates strongly with the presence of chronic gastritis, and significantly with gastric and duodenal ulceration. The best diagnostic approach is the combination of a rapid urease detecting test and histology. C.p. infection is of long duration and difficult to eliminate. The most effective treatment for C.p. infection remains BSS as single agent.
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PMID:Epidemiology and treatment of gastric Campylobacter pylori infection: more questions than answers. 198 7

Campylobacter pylori is a bacterium that inhabits gastric mucosa. It causes chronic active gastritis and is highly associated with duodenal ulcer. Campylobacter pylori has a urease enzyme (not present in man), which allows diagnosis by a [14C]urea breath test. We compared two noninvasive tests, the breath test and serum ELISA, to biopsy and histologic diagnosis. Twenty-two patients who underwent gastroduodenoscopy for evaluation of possible peptic ulcer disease entered the study. The breath test detected the organism in eight of eight patients biopsy-positive for the organism (sensitivity 100%). The breath test was negative in 12 of the 14 patients who were biopsy-negative (specificity 86%). The ELISA was performed in 14 patients. It was positive in 5 of 5 patients biopsy-positive for the organism (sensitivity 100%) and negative in 7 of 9 patients who were biopsy-negative (specificity 78%). We conclude that both the ELISA and the [14C]urea breath test are excellent noninvasive methods to detect Campylobacter pylori. However, only the breath test is suitable for following the response to treatment, as it detects the presence of the organism rather than an immune response to it.
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PMID:Diagnosis of Campylobacter pylori gastritis. 198 94

The potential of Helicobacter pylori to degrade gastric mucus was examined. Colonies of H pylori cultured from antral mucosal biopsy specimens of patients with non-autoimmune gastritis were washed with sterile saline, passed through a sterilisation filter, and the filtrate examined for urease, protease, and mucolytic activity. The filtrate failed to hydrolyse bovine serum albumin, or to degrade stable mucus glycoprotein structures of high particle weight that had been separated from human gastric mucus on Sepharose 2B. The high particle weight mucus glycoprotein was, however, extensively degraded when incubated with H pylori filtrate (which possessed urease activity) in the presence of 2 M urea, to release fragments of Mr approximately 2 X 10(6). The high particle weight mucus glycoprotein was also broken down to a comparable extent when incubated with Jack bean urease in the presence of 2 M urea, or 1 M ammonium carbonate, or 40 mM carbonate-bicarbonate buffer (pH 8.7), but not when treated with 4 M urea alone, or Jack bean urease alone. These results indicate that the loss of high particle weight mucus glycoprotein in gastric mucus from patients with gastritis and gastric ulcers is unlikely to be due to the mucolytic action of an extra-cellular protease produced by H pylori, but it may result from the destabilising effects of a carbonate-bicarbonate buffer, generated at the mucosal surface when H pylori urease hydrolyses transuded plasma urea.
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PMID:Breakdown of gastric mucus in presence of Helicobacter pylori. 199 34

Production of a potent urease has been described as a trait common to all Helicobacter pylori so far isolated from humans with gastritis as well as peptic ulceration. The detection of urease activity from genes cloned from H. pylori was made possible by use of a shuttle cosmid vector, allowing replication and movement of cloned DNA sequences in either Escherichia coli or Campylobacter jejuni. With this approach, we cloned a 44-kb portion of H. pylori chromosomal DNA which did not lead to urease activity when introduced into E. coli but permitted, although temporarily, biosynthesis of the urease when transferred by conjugation to C. jejuni. The recombinant cosmid (pILL585) expressing the urease phenotype was mapped and used to subclone an 8.1-kb fragment (pILL590) able to confer the same property to C. jejuni recipient strains. By a series of deletions and subclonings, the urease genes were localized to a 4.2-kb region of DNA and were sequenced by the dideoxy method. Four open reading frames were found, encoding polypeptides with predicted molecular weights of 26,500 (ureA), 61,600 (ureB), 49,200 (ureC), and 15,000 (ureD). The predicted UreA and UreB polypeptides correspond to the two structural subunits of the urease enzyme; they exhibit a high degree of homology with the three structural subunits of Proteus mirabilis (56% exact matches) as well as with the unique structural subunit of jack bean urease (55.5% exact matches). Although the UreD-predicted polypeptide has domains relevant to transmembrane proteins, no precise role could be attributed to this polypeptide or to the UreC polypeptide, which both mapped to a DNA sequence shown to be required to confer urease activity to a C. jejuni recipient strain.
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PMID:Shuttle cloning and nucleotide sequences of Helicobacter pylori genes responsible for urease activity. 200 95

An immunofluorescence assay (IFA) for the detection of immunoglobulin G antibodies directed against Helicobacter pylori was evaluated by comparing 20 serum specimens from patients with a positive urease test on biopsy material and 20 serum specimens from patients with a negative test and with defined clinical symptoms. The resulting anti-H. pylori titers were classified as follows: negative, less than or equal to 64; borderline, 128; and positive, greater than or equal to 256. By using these criteria, the IFA was subsequently tested, using 100 serum specimens from patients with gastric complaints. Overall, the titers were 71% positive, 10% borderline, and 19% negative. Depending on the patients' biopsy urease test results, the sensitivity and specificity of the assay were calculated to be 96%. Furthermore, these sera were classified into three subgroups on the basis of clinical manifestations: gastritis with 74% positive and 10% borderline titers, duodenal ulcer with 84% positive and 4% borderline titers, and gastric ulcer with 52% positive and 16% borderline titers. A serologic follow-up study was carried out with three patients with gastric ulcers who had been treated with colloidal bismuth subcitrate for 4 weeks and erythromycin for the final 2 weeks. The results indicate that a significant decrease in titer could be expected within 9 to 12 months after successful therapy, as determined by repeated negative CLO tests. Absorption experiments demonstrated that possible cross-reactivity between H. pylori and C. jejuni did not influence serodiagnosis.
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PMID:Evaluation of an immunofluorescence assay for specific detection of immunoglobulin G antibodies directed against Helicobacter pylori, and antigenic cross-reactivity between H. pylori and Campylobacter jejuni. 200 40


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