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)

The ideal approach for the initial diagnosis of Helicobacter pylori infection is to perform an endoscopy to obtain biopsy specimens for histology and culture. Histology allows classification of any gastritis lesions present and may have prognostic value, and culture enables susceptibility testing of antimicrobial agents to direct proper treatment. Biopsy specimens must also be taken from the corpus if the patient was pretreated with proton pump inhibitors. The cost of these tests and the delay in receiving results limits their use in clinical practice. Therefore, the urease test, a quick and inexpensive test, is used to detect the presence of H. pylori and constitutes the basic invasive test for H. pylori. A new urease test based on a strip instead of an agar disk may be the test of choice in the future, because of its increased sensitivity and 2-hour delay (instead of 24 hours) in obtaining the result. In some countries, because of the cost, endoscopy will be used in selected patients only, either because of alarm symptoms or age > 45 years, which is considered a threshold for gastric cancer risk. In other patients, the noninvasive tests will be used. The cost of serology makes it more attractive compared with the urea breath test. Currently, there are accurate enzyme-linked immunosorbent assay tests that can be performed in any laboratory and that provide precise and quick diagnoses. In the event of a doubtful result, an immunoblot can be performed, as is the case for other infections. Patient follow-up after treatment provides a different situation because bacterial load is usually lower. A noninvasive test should be performed, and only the urea breath test can be used within the timing originally proposed to test eradication efficacy (i.e., 4-6 weeks after treatment). If the result is positive, susceptibility testing is required before administering a second course of treatment. The increasing use of antimicrobial agents to treat H. pylori is likely to result in antimicrobial resistance, requiring that bacteriologic surveillance programs be implemented. There are numerous research projects ongoing in this area, and one can expect that improved methods, such as colorimetric polymerase chain reaction (PCR) and improved antibody tests, will also be used in the future.
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PMID:How should Helicobacter pylori infection be diagnosed? 939 68

Helicobacter pylori has been implicated in the etiology of peptic ulcer disease, chronic gastritis, gastric carcinoma, and gastric mucosa-associated lymphoid tissue lymphoma. Although significant progress has been made in treating this infection with combinations of either antimicrobial agents or antimicrobial agents plus proton pump inhibitors, these antimicrobial-based treatments continue to be suboptimal. Over the past few years it has become increasingly recognized that direct mucosal immunization can induce protection from infection at mucosal surfaces. Therefore, prevention of H. pylori infection by oral immunization is an alternative approach for the control of H. pylori disease. Using the Helicobacter felis mouse model or H. pylori mouse model, both prophylactic and therapeutic oral immunizations have been shown to be effective against H. pylori. In addition, several H. pylori proteins have been identified as potential candidate vaccines, and a phase 1 clinical trial has been completed that demonstrates the safety and tolerability of urease as a vaccine antigen. Such antigens in combination with a safe mucosal adjuvant could be used in the form of an oral vaccine administered during childhood before exposure to H. pylori to prevent infection. In addition, therapeutic immunization alone or as an adjunct to antimicrobial therapy may be capable of achieving a cure rate approaching 100%.
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PMID:What is the role for vaccination in Helicobacter pylori? 939 76

Treatment with the proton pump inhibitor (omeprazole) and single antibiotic (amoxycillin), two synergistic compounds, can cure Helicobacter pylori (H. pylori) infection, but this therapy is not as effective as had been expected. However, some studies show promising results. The aim of our study was to evaluate the effect of two weeks dual-therapy with omeprazole (O) and amoxycillin (A) on gastric (GU) and duodenal ulcer (DU) patients: ulcer healing, eradication of the H. pylori and recurrence rate of the ulcer. We studied 216 patients (aged 18-70) endoscopically proven GU (58 patients) and DU (158 patients). Rapid urease test from the two antrum biopses and two antral and two corporeal biopses using Giemsa stain method for confirmation of the H. pylori infection were used. The patients were treated with omeprazole 20 mg BID and amoxycillin 1.0 g BID for 2 weeks and investigated every 4 months during 2 years. Clearance effect of Hp infection was achieved in 65.1% GU and 66.4% DU patients. Eradication ("check point" after 4 months) in 43% DU and 56.6% GU patients was confirmed. Reinfection rate was found in 16% during 2 years. We conclude--dual-therapy (O and A) is not sufficiently effective to be recommended as an anti-H. pylori treatment. H. pylori eradication prevents recurrence of peptic ulcer and is an important issue in attempts to achieve permanent ulcer healing.
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PMID:Multicenter evaluation of dual-therapy (omeprazol and amoxycillin) for Helicobacter pylori-associated duodenal and gastric ulcer (two years of the observation). 944 60

The eradication of Helicobacter pylori is at present widely recognized as the adequate therapeutic approach for gastric and duodenal ulcers in infected patients. In those with dyspepsia but no ulcer as well as in those with type B chronic gastritis, eradication remains controversial. It is difficult to have a clear opinion on the advantages and disadvantages of the numerous existing therapies. Therefore, a systematic review of published treatments has been made by the authors. Ideally, the eradication treatment of H. pylori should have the following advantages: 1. eradication superior to 90%, 2. simplicity, 3. short duration, 4. safety, 5. low cost, 6. reproducibility of results. Dual therapies (2 antibiotics or a proton pump inhibitor in combination with an antibiotic) rarely allow an eradication greater than 90% and the results have poor reproducibility. Consequently, they do not represent an ideal anti-H. pylori treatment. Triple therapies come closer to the requirements for an ideal treatment, with eradication rates generally close to 90%, varying little between studies and the countries in which they were performed. The triple therapy bismuth-imidazole-tetracycline (or amoxicillin) still represents for many authors the standard reference therapy. It has the advantage of low cost, high efficacy and widespread use. It is the therapy that has been the most studied. However, the increasing emergence of strains resistant to imidazoles, the complexity of the treatment (10 to 12 tablets per day), the numerous adverse effects and the lack of availability of bismuth salts in certain countries has led to the elaboration of therapeutic schemes combining an antisecretory drug with 2 antibiotics. Among these, the combination PPI-clarithromycine-imidazole during 7 days represents the most studied triple therapy of short duration for some authors, it already represents a new standard. However, the efficacy of this therapy seems dependent on the sensitivity of the bacteria to imidazoles. Consequently, this combination cannot be considered as the ideal anti-H. pylori treatment in the areas where the prevalence of strains resistant to imidazoles is high. The association PPI-clarithromycine-amoxicillin appears on the contrary to be very effective against strains resistant to metronidazole and therefore could constitute the treatment of choice in population with high prevalence of such strains. Great hope is currently surrounding the finalization of a vaccine directed against the urease of the bacteria. This approach would allow both the treatment and the prevention of Helicobacter pylori infection on a large scale.
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PMID:The eradication treatments of Helicobacter pylori. 953 66

The purposes of this study were to assess the efficacy of a 1-week proton pump inhibitor (PPI)-based triple therapy after failure of dual therapy in Helicobacter pylori eradication, and to compare the effectiveness of clarithromycin and metronidazole in this regimen. Between January 1996 and March 1997, 67 patients with persistent H. pylori infection after a 2-week course of dual therapy (amoxicillin plus omeprazole) were enrolled. They were randomly assigned to receive amoxicillin (1000 mg twice daily) and omeprazole (20 mg twice daily) plus either metronidazole (500 mg twice daily) or clarithromycin (250 mg twice daily). Endoscopy was performed in each patient to assess the status of H. pylori using the rapid urease test (CLOtest) and the histologic findings before dual therapy, after dual therapy, and after triple therapy. H. pylori isolates were tested for antibiotic resistance when triple therapy failed. The 1-week triple therapy was well tolerated in both groups with no adverse effects severe enough to cause withdrawal from the trial. Residual H. pylori was eradicated in 94% (33/35) of patients in the clarithromycin group and 84% (27/32) in the metronidazole group; the difference was not statistically significant. All seven patients in whom triple therapy failed were infected with metronidazole-resistant isolates and two also had clarithromycin-resistant isolates. This 1-week triple therapy is safe and effective in eradicating residual H. pylori after dual therapy failure. Failure of the rescue regimen is related to antimicrobial agent resistance. Because of the high metronidazole resistance rate in Taiwan, clarithromycin appears to be more promising than metronidazole for the control of H. pylori.
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PMID:One-week proton pump inhibitor-based triple therapy eradicates residual Helicobacter pylori after failed dual therapy. 958 78

In almost all eradication regimens, which contain antibiotics and bismuth derivatives, the administration of acid suppressing drugs for 4-6 weeks is recommended for healing of duodenal ulcer. The aim of this multicenter double blind study is to elucidate the effect of two classic antibiotics tetracycline (CAS 60-54-8) and metronidazole (CAS 443-48-1) alone or combined with ranitidine (CAS 66357-35-5) on the healing of duodenal ulcer and eradication of Helicobacter Pylori. Patients with duodenal ulcer were randomized to two treatment groups: group A received either ranitidine 4 x 150 mg or tetracycline 4 x 500 mg or metronidazole 3 x 250 mg for 2 weeks. Group B received 4 x placebo + tetracycline and metronidazole as in group A for 2 weeks. A final endoscopy was performed after 8 weeks. Four biopsy specimens were obtained from the antrum (two) and corpus (two) for both urease test and hematoxylin stain for detection of H. pylori. Out of 201 patients entering the study 156 completed the study (78 in A and 78 in B). The healing rate of duodenal ulcer was 98.7% in group A and 97.5 in group B. The eradication rate was only 33.3% in group B but 64% in group A (p < 0.001), when additionally ranitidine was given. The present study shows that treatment with the two antibiotics tetracycline and metronidazole alone results in a very low H. pylori eradication, but almost complete healing of duodenal ulcer after 8 weeks. Prolonged administration of antisecretory drugs in eradication regimens containing two antibiotics is not necessary for duodenal ulcer healing. However, the addition of H2-receptor antagonists or proton pump inhibitors to antibiotics increases the eradication rate.
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PMID:Efficacy of tetracycline and metronidazole alone or with ranitidine on the healing of duodenal ulcer and eradication of Helicobacter pylori. A randomized controlled multicenter study. Tetra-Metro-Ran Study Group. 968 28

The treatment of peptic ulcers has been revolutionized by the discovery that Helicobacter pylori (H. pylori) bacteria is a causative agent for ulcer formation. However, when patients present with dyspepsia or epigastric discomfort, more than 80% of patients will not have ulcer disease and empiric treatment of H. pylori is not recommended for these patients. Eradication of H. pylori has not been demonstrated to improve the symptoms of non-ulcer dyspepsia compared with non-ulcer dyspepsia patients treated with placebo. Therefore, we recommend that patients should first be evaluated for peptic ulcers with endoscopy or upper gastrointestinal series before the diagnosis and treatment of H. pylori. Generally, the treatment of H. pylori should be limited to patients with peptic ulcers, mucosal-associated lymphoid tissue lymphomas, and gastric cancers. Most diagnostic tests for H. pylori, including quantitative IgG antibody, urea breath tests, rapid urease tests (CLO), tests of gastric mucosal biopsies, and staining of gastric mucosal biopsies, have equivalent diagnostic characteristics. Therefore, the choice of diagnostic test for H. pylori should be based on cost, ease of use, and lack of complications. Multiple antibiotic regimens are available for the treatment of H. pylori. Triple antibiotic therapy is the least expensive but has the highest rate of side effects and the least compliance. Combining a proton pump inhibitor with clarithromycin and another antibiotic will eradicate H. pylori with fewer side effects and better compliance but this is the most expensive antibiotic regimen.
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PMID:Acid peptic diseases in the era of Helicobacter pylori. 970 81

It has been suggested that profound acid inhibition by proton pump inhibitors affects the accuracy of H. pylori detection. This report aims to evaluate H. pylori status during treatment with four different invasive detection methods and to investigate if histopathological alterations during treatment can be used as an early marker for H. pylori eradication. Twenty-eight H. pylori-positive patients were studied randomized into two treatment groups: 14 patients received omeprazole, 20 mg plus amoxicillin 1,000 mg b.i.d (OA), and 14 patients received omeprazole, 20 mg and placebo b.i.d (OP) for 14 days. Biopsies from antrum and corpus of the stomach were collected on days 0, 10 and 42. H. pylori status was based on rapid urease test, cultivation, histology, and polymerase chain reaction (PCR). The biopsies were also graded according to the Sidney classification. In the OP and the OA group, 17% (2/12) and 92% (12/13) of the patients were H. pylori negative when tested during treatment (day 10). Four weeks after treatment none of the patients (0%) in the OP group and 61% (8/13) in the OA group had their H. pylori infection eradicated. PCR was up to 34% more sensitive than the other tests to detect H. pylori during treatment. There was a decrease in histological inflammation and activity in the antrum already during treatment in the OA group, but the decrease did not discriminate for successful treatment. During treatment with omeprazole alone or in combination with amoxicillin, H. pylori detection is impaired regardless of the detection method used. However, PCR appears to be more sensitive than other tests. Early changes in the histological appearance of the gastric mucosa do not predict H. pylori treatment outcome.
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PMID:The value of different detection methods of Helicobacter pylori during treatment. 975 75

The ability of Helicobacter pylori to survive in the varying acidity of the stomach is considered to be linked to its ability to maintain a tolerable pH in its periplasmic space by acid dependent activation of internal urease activity. Whereas survival of H pylori can occur between a periplasmic pH of 4.0 to 8.0, growth can only occur between a periplasmic pH of 6.0 to 8.0. When urease activity is only able to elevate periplasmic pH to between 4.0 and 6.0, the organisms will survive but not divide. In the absence of division, antibiotics such as clarithromycin and amoxycillin are ineffective. Proton pump inhibitors, by elevating gastric pH, would increase the population of dividing organisms and hence synergise with these antibiotics.
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PMID:The life and death of Helicobacter pylori. 976 42

The proton pump inhibitors (PPIs) omeprazole, lansoprazole, and pantoprazole are widely used as antisecretory drugs and, in association with antibiotics, for the treatment of Helicobacter pylori infections. PPIs possess antibacterial activity against H. pylori in vitro, and may also exert an anti-inflammatory effect by interfering with the cellular immune response to infection. Their antimicrobial activity is selective for H. pylori. Lansoprazole is the most effective, although its bactericidal activity is similar to that of omeprazole. Pantoprazole is the least effective. The mechanisms that account for the antibacterial effects of PPIs may depend on a structural similarity of PPIs to antibiotics which are active against H. pylori, on the inhibition of bacterial urease exerted by PPIs, or on the possible interaction of PPIs with bacterial ATPases that regulate the transmembrane ion flux. Recent studies have shown that PPIs have anti-inflammatory actions and can interfere with the host-bacteria interactions. Lansoprazole can bind to polymorphonuclear leukocytes that infiltrate the gastric mucosa colonized by H. pylori and can thus inhibit the oxidative burst of activated inflammatory cells. In an in vivo study, lansoprazole reduced the degree of activity of histologic gastritis independently of the presence of H. pylori. In another study, omeprazole was capable of inhibiting the cytotoxic activity of NK T cells. Investigation of PPI interactions with H. pylori activities and the cellular immune response to the infection may help us to understand the pathogenic mechanisms of H. pylori-associated diseases and enable clinicians to better treat them.
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PMID:Helicobacter pylori infection, chronic gastritis, and proton pump inhibitors. 987 16


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