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:6.3.4.6 (urease)
7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

25 patients with Helicobacter pylori-associated active duodenal ulcer disease (bleeding: n = 5, penetrating: n = 1, stenosis of the bulb: n = 4, frequent ulcer relapse: n = 18) were treated with 3 x 600 mg bismuth subsalicylate (BSS), 3 x 400 mg metronidazole and 3 x 500 mg tetracycline in addition to 300 mg ranitidine. 23 out of 25 patients (92%) proved to be Helicobacter pylori-negative four weeks after cessation of study medication as judged from negative urease test, specific culture and histology after modified Giemsa staining. 24/25 ulcers (96%) had healed after six weeks. In one patient on NSAIDs a small duodenal ulcer was detected on the final endoscopic examination despite successful Helicobacter pylori eradication. Twelve out of 25 (48%) patients complained side effects that did not lead to discontinuation of therapy. In conclusion, oral triple therapy with BSS, metronidazole and tetracycline is highly effective in Helicobacter pylori eradication, but there was a rather high rate of more or less serious side effects, diminishing the attractiveness of this therapeutic regimen.
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PMID:[Oral triple therapy for eradication of Helicobacter pylori in duodenal ulcer disease]. 832 16

To evaluate the sensitivity of a polymerase chain reaction (PCR) assay using nested primers in detecting Helicobacter pylori, gastric tissue biopsy specimens were collected on endoscopy from 17 patients with a duodenal ulcer. DNA was extracted by phenol/chloroform treatment or boiling in water, and then subjected to a nested PCR using two primer pairs from the urease gene of Helicobacter pylori. Fourteen of the 17 patients were positive for Helicobacter pylori using DNA samples extracted by either method. The PCR results correlated well with the results of an enzyme immunoassay to detect IgG antibody. However, there were two culture negative patients. The three PCR negative patients were both culture negative and serologically negative. DNA from 9 of the 14 patients was randomly selected and subjected to semiquantification by serial dilutions, and then PCR. The results showed that phenol/chloroform extraction yielded 10-1000 times more DNA than the boiling method. It is concluded that the PCR assay is a rapid and sensitive method for detecting Helicobacter pylori, and that phenol/chloroform extraction is superior to simple boiling in obtaining DNA samples for PCR.
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PMID:Detection of Helicobacter pylori in gastric biopsy tissue by polymerase chain reaction. 835 5

A controlled, prospective clinical trial of colloidal bismuth subcitrate (CBS), ranitidine and ranitidine plus metronidazole for the treatment of duodenal ulcer (DU) is reported here, with evaluation of the possible pathogenic role of Helicobacter pylori (HP) on DU in a six-month follow-up. A total of 42 patients with active DU on endoscopy were randomly selected to receive oral CBS (300 mg 1 hour before each meal, and at bedtime, n = 16), ranitidine (150 mg bid; n = 12) or ranitidine (150mg b.i.d.) plus metronidazole (250 mg t.i.d; n = 14) treatment for one month. Ulcer healing was endoscopically evaluated. Healed patients received another two-week treatment; unhealed subjects received another one-month treatment with the same agents. Healed patients were followed endoscopically at 1, 3, and 6 months after the cessation of medication without maintenance therapy. Unhealed or relapsed subjects were excluded. To assess HP status, during each endoscopy two prepyloric mucosal biopsies were taken for urease testing and culture of HP. The prevalence of HP in patients with DU was 95.2%. Data showed that those treated with CBS had a lower DU healing rate than those treated with ranitidine or ranitidine plus metronidazole after the one-month treatment, but there was no statistical significance in the DU healing rates after the two-month treatment, and at follow-up six months after the cessation of medication. After one month of treatment those treated by CBS showed the highest rates of HP clearance on gastric antral mucosa among the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Colloidal bismuth subcitrate, ranitidine, and ranitidine plus metronidazole in the treatment of duodenal ulcer and Helicobacter pylori infection: a controlled and prospective study. 836 76

Thirty-three consecutive patients with idiopathic gastric acid hypersecretion (defined as a basal acid output > 10.0 meq/hr with a normal fasting serum gastrin level and negative secretin stimulation test) who were being treated for duodenal ulcer disease and other acid-peptic disorders were evaluated for the presence of Helicobacter pylori by means of a rapid urease test. Fourteen patients had duodenal ulcer and 19 had other acid-peptic disorders (gastroesophageal reflux in 14, including six with Barrett's esophagus; four with nonulcer dyspepsia; and one with erosive gastritis). Helicobacter pylori was present in 12 of the 14 ulcer patients (86%) compared to only two of the 19 nonulcer patients (11%) (P < 0.0001). The distribution of basal acid output for patients with duodenal ulcer was similar to that for nonulcer patients, and no significant difference in the mean basal acid output was found among Helicobacter pylori-positive compared to Helicobacter pylori-negative patients. Seven of the duodenal ulcer patients with a basal acid output greater than 15.0 meq/hr were Helicobacter pylori-positive, suggesting that the organism can withstand even extreme levels of gastric acidity. In conclusion, this study demonstrates that the prevalence of Helicobacter pylori infection in patients with duodenal ulcer disease associated with idiopathic gastric acid hypersecretion is not different from a majority of ulcer patients with normal acid secretory profiles and offers additional evidence that extreme levels of gastric acid are not bactericidal for the organism.
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PMID:Helicobacter pylori in duodenal ulcer patients with idiopathic gastric acid hypersecretion. 842 Jul 45

The objective of this study was to evaluate the accuracy of an indirect immunofluorescence (IIF) test for serodiagnosis of Helicobacter pylori infection in children and to determine how the test is affected by the presence of antibodies against Campylobacter jejuni. We studied 65 consecutive children (two with endoscopically confirmed duodenal ulcer) and a series of 18 children with duodenal ulcer. Thirty children were H. pylori negative, as determined by culture, by the preformed urease test, and by carbolfuchsin-stained smears. The microorganism was identified by microbiological methods in 35 of the 65 (53.85%) consecutive patients studied and in all children with duodenal ulcer. The titer of the IIF test was > or = 1:20 in the sera of all children with duodenal ulcer and in the sera of 30 of 33 H. pylori-positive children without duodenal ulcer. No H. pylori-negative children had titers > 1:10. A serum dilution of 1:20 discriminated between H. pylori-infected and noninfected children. Absorption with C. jejuni did not change the levels of IgG against H. pylori. When five patients who had been successfully treated with metronidazole, amoxycillin, and furazolidone for 7 days were retested, a slight decrease in anti-H. pylori IgG levels was noted from the third month on. The decrease was more significant 9 months after the eradication of the microorganism.
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PMID:Serodiagnosis of Helicobacter pylori infection in children by an indirect immunofluorescence test. 849 50

Using different bacteriological (urease test, Gram staining and culture) and histological (Steiner staining and modified Giemsa staining) techniques, we searched for the presence of Helicobacter pylori in the gastric antrum of 200 dyspeptic Brazilian patients (106 females and 94 males aged 19 days to 81 years). The presence of bacteria was then correlated with the endoscopic and histological findings. H. pylori was present in 59.5% of the population studied. In Brazil, colonization occurs early, involving 37% of the dyspeptic population by 20 years of age. The presence of H. pylori in the gastric antrum was strongly associated with duodenal ulcer (P < 0.001) and a normal endoscopic examination did not exclude the possibility of colonization of the gastric antrum by H. pylori. The most sensitive test was the preformed urease test (89%). We conclude that more than one diagnostic method should preferably be used for the detection of H. pylori and that the presence of H. pylori is closely correlated with active chronic gastritis (P < 0.001).
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PMID:Helicobacter pylori in dyspeptic children and adults: endoscopic, bacteriologic and histologic correlations. 852 59

Helicobacter pylori is a Gram-negative bacterium with man as the unique reservoir and where the niche is the stomach. Transmission between individuals could be by fecal and oral route. In the stomach, the bacterium is mainly located at the mucus level and adhere to antral cells which are the privileged target. Within the colonized mucosa, H. pylori generates or secretes different deleterious compounds against the epithelial cells: urease, hydrolyzing urea into ammonia, a cytotoxic agent: monochloramine also cytotoxic, various enzymes and a vacuolyzing cytotoxin; all of these also contribute to the pathogenic potential. In addition the associated inflammatory reaction probably plays a part in the lesion process. One important consequence is peptic ulcer disease and particularly duodenal ulcer which can further degenerate into a precancer lesion and to a lesser extent some dyspeptic syndromes. Bacterial eradication can be obtained by the combination of an antisecretory drug with an antibiotic. Macrolides have a good activity against this bacterium. The azithromycin MIC50 is 0.12 mg/l. A bactericidal activity is observed at concentrations equal or higher than 0.10 mg/l. After a single dose of 500 mg, azithromycin concentrations are 0.48 micrograms/g in the mucus and 4 micrograms/g in the gastric tissue. Concentrations persist for a long time, due to long half life (3 days). In pilot clinical trials, with a tritherapy combining azithromycin with metronidazole and omeprazole, 80% of bacterial eradication was obtained. These promising need to be validated by larger clinical trials.
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PMID:[Helicobacter pylori and azithromycin]. 853 82

A PCR assay for the detection of Helicobacter pylori in gastric biopsy specimens with specific primers for ureC gene amplification (herein referred to as ureC PCR) was compared with other routine invasive methods (culture, the rapid-urease test, and Giemsa staining of histological sections) with samples from a group of 104 consecutive dyspeptic patients. Bacteria were found in 40 (38.5%), 38 (36.5%), 36 (34.6%), and 35 (33.7%) of the patients by ureC PCR, culture, the rapid-urease test, and Giemsa stain, respectively. Sixty-three patients had negative cultures, negative histological examinations, and negative rapid-urease test results, and 61 of these patients were also negative by ureC PCR. ureC PCR detected H. pylori in two culture-negative patients. In parallel, a PCR-based assay to detect the H. pylori cytotoxin-associated antigen (cagA) gene, a putative virulence gene, was also developed. To assess the likelihood of detection of H. pylori genes directly from gastric biopsy samples and from the corresponding H. pylori isolates, specimens from 31 patients were subjected to PCR with ureC- and cagA-targeting primers. All 31 biopsy specimens and the corresponding H. pylori isolates were positive in the ureC PCR. H. pylori strains that were cagA positive also gave positive cagA PCR fragments with biopsy specimens from the same patients. All ureC PCR-positive patients were examined; biopsy specimens from 10 of 11 (91.7%) duodenal ulcer patients harbored H. pylori cagA-positive strains, whereas 19 of26 (73%) of those from patients with chronic gastritis only were found to be cagA positive. These findings indicate first that ureC PCR is at least as sensitive as culture for diagnosing H. pylori infection and second that the presence of the H. pylori cagA gene can also be detected directly in biopsy specimens by PCR amplification.
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PMID:Diagnosis of Helicobacter pylori infection by PCR: comparison with other invasive techniques and detection of cagA gene in gastric biopsy specimens. 856 18

Helicobacter pylori, the etiologic agent of gastritis and peptic ulceration, may infect the gastric mucosa of over half of the world's population. Despite the high infection rate, symptomatic disease beyond gastritis (characterized by gastric or duodenal ulcer) is noted in a small, but nevertheless significant, fraction of this population. What defines an H. pylori strain as a pathogen that can cause the more serious clinical manifestations? In addition to the more well recognized virulence determinants, such as urease, flagella, and vacuolating cytotoxin, evidence is emerging that the more virulent strains possess well defined segments of DNA. These "pathogenicity islands" include cytotoxin-associated gene A and encode proteins involved in signal transduction events that may facilitate intimate attachment to host cells, cytoskeletal rearrangement via actin polymerization, and host cell protein phosphorylation.
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PMID:Defining Helicobacter pylori as a pathogen: strain heterogeneity and virulence. 864 79

Helicobacter pylori has been implicated as an agent in the pathogenesis of antral gastritis, gastric and duodenal ulcer and probably in gastric cancer. The C13 urea breath test is a diagnostic method quick to perform, sensitive, reliable and non invasive. It is based on the presence of Helicobacter pylori urease activity, which permits to detect it in the infected mucosa. A substrate (urea) labelled with Carbon 13 is administered to the patient and exhaled breath is collected to detect the possible catabolism product (CO2 labelled with C13). In the European protocol, patients in fasting condition are given a test meal to delay gastric emptying and five minutes later a solution which contents 100 mg of C13 labelled urea. Breath samples are collected before and 30 minutes after urea was given. In our first year of experience, 363 patients with Helicobacter pylori infection detected by histology or urease were studied by C13 urea breath test, with a sensitivity and specificity of 95 and 96%. False negatives may occur if the test is used after antibiotics and other antiulcer drugs. Its main indication is to monitor eradication therapy after treatment. Its possible use as a quantitative test still remains unclear.
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PMID:[C13 urea breath test in the diagnosis of Helicobacter pylori infection in the gastric mucosa. Validation of the method]. 864 14


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