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)

Helicobacter pylori has been identified as a dominant factor in the pathogenesis of duodenal ulcer. The aim of this study was to examine peripheral blood and gastric lymphocyte proliferation and cytokine production in patients with H pylori colonisation. Sixty five dyspeptic patients attending for endoscopy were studied; 35 of these were H pylori positive and 30 H pylori negative as assessed by culture, histology, and rapid urease test. H pylori antigen was capable of stimulating peripheral blood lymphocyte proliferative responses even in H pylori negative patients. Peripheral blood lymphocyte proliferative responses to H pylori (but not to purified protein derivative or phythaemagglutinin) were significantly lower in H pylori positive than H pylori negative patients. Similarly, antigen specific proliferative responses and interferon gamma production by gastric lamina propria lymphocytes were also depressed in H pylori positive patients compared with H pylori negative patients. CD8 and CD22 positive lamina propria lymphocytes were increased in H pylori positive patients. These data show that antigen specific responses to H pylori are significantly lower in H pylori positive patients and could indicate activation of antigen specific suppression.
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PMID:Gastric T lymphocyte responses to Helicobacter pylori in patients with H pylori colonisation. 795 91

Colonization of Helicobacter pylori (HP) beneath the protective film of gastric mucus enables the organism to survive in the hostile environment of the gastric mucosa. N-acetylcysteine (NAC), a sulfhydryl compound with potent mucolytic activity, induces a reduction of gastric barrier mucus thickness of about 75% and reduces mucus viscoelasticity. We therefore tested the hypothesis whether better eradication results could be achieved by addition of NAC to omeprazole/amoxicillin (OME/AMOX). 34 HP positive outpatients with endoscopically documented recurrent duodenal ulcer were included in an ongoing, prospective, randomized trial. Exclusion criteria were: alcoholism, previous gastric surgery, or intake of antibiotics, OME, bismuth salts, corticosteroids or NSAIDs within 4 weeks before study entry. Patients currently smoking > 10 cigarettes/day were classified as smokers. HP infection was confirmed by histology (3 biopsy specimens from gastric antrum and 2 from gastric body; H&E, Giemsa) and at least positive rapid urease test or culture. All 34 patients underwent ulcer therapy with OME (20 mg per day) for 20 days (d 1-20). Group A: in 17 patients (5 females, 12 males, mean age 46 [29-74] years; 8 smokers, 9 nonsmokers) the subsequent eradication therapy, consisting of oral OME (40 mg bid) and AMOX solute (750 mg tid) for 10 days, was combined with NAC solute (2 x 600 mg bid (d 21-30). Group B: 17 patients (2 females, 15 males, mean age 39 [19-70] years; 11 smokers, 6 nonsmokers) underwent eradication therapy without NAC (d 21-30). Control endoscopy was done after a minimal interval of 30 days from the end of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Omeprazole/amoxicillin: improved eradication of Helicobacter pylori in smokers because of N-acetylcysteine]. 809 Nov 67

The efficacy of high dose omeprazole/amoxicillin (OME/AMOX) for eradication of Helicobacter pylori (HP) is controversial. Reported eradication rates range from 0% to 90%. Different therapy schedules and unknown factors may be crucial; in particular, pretreatment with OME has been thought to endanger HP eradication by subsequent OME/AMOX. Preliminary findings suggested that smoking may impair eradication with OME/AMOX. The aims of this study were (1) to establish whether HP eradication rates differ depending on whether eradication with OME/AMOX was performed before or after ulcer therapy with OME, (2) to determine whether smoking impairs HP eradication by OME/AMOX and (3) to evaluate the efficacy of OME/AMOX in our population. 52 HP positive outpatients with endoscopically documented recurrent duodenal ulcer were included. Exclusion criteria were: alcoholism, previous gastric surgery, or intake of antibiotics, OME, bismuth salts, corticosteroids and NSAIDs within four weeks before study entry. Patients currently smoking > 10 cigarettes/day were classified as smokers. HP infection was confirmed by histology (3 biopsy specimens from the gastric antrum and 2 from the gastric body; H&E, Giemsa) and at least positive rapid urease test (CLO) or culture. Eradication therapy consisted of oral OME (40 mg bid) and AMOX solute (750 mg tid) for 10 days (OME/AMOX). This therapy preceded (group A) or followed (group B) ulcer therapy with OME (20 mg per day for 20 days). In group A 17 patients (2 females, 15 males, mean age 39 [19-70]; 11 smokers, 6 nonsmokers) underwent ulcer therapy with OME (d 1-20) before OME/AMOX d 21-30).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Omeprazole/amoxicillin: impaired eradication of Helicobacter pylori in smoking but not in premedication with omeprazole]. 809 Nov 68

One hundred and ninety-six symptomatic Saudi patients with dyspepsia underwent gastroscopy, and multiple biopsies were taken from the antrum of the stomach for identification of Helicobacter pylori. Three methods were studied for diagnosis of Helicobacter pylori, including urease test, culture and histopathology. The commonest gastroscopic findings were gastritis in 82 patients (41.84%) and duodenal ulcer in 40 patients (20.41%). Among the 196 patients, Helicobacter pylori was identified by histopathology in 145 patients (73.98%), the urease test was positive in 126 patients (64.29%), and a positive culture was obtained in 102 patients (52.04%). These results show that there is a high incidence of Helicobacter infection among Saudi patients with peptic ulcer disease or non-ulcer dyspepsia. Helicobacter pylori identification was more successful by histopathology than by the urease test or culture.
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PMID:Helicobacter pylori: incidence and comparison of three diagnostic methods in 196 Saudi patients with dyspepsia. 817 15

In a prospective study we examined 20 Helicobacter pylori (HP)-positive duodenal ulcer patients (5 female, 15 male; age 26-70 [mean 43] years), 20 HP-positive patients with non-ulcer dyspepsia (10 female, 10 male; age 26-79 [mean 48] years) and 10 HP-negative patients with non-ulcer dyspepsia (5 female, 5 male; age 21-76 [mean 45] years) during upper GI-endoscopy. HP was detected by histology (H&E, Giemsa), rapid urease test (CLO) and serology (Cobas Core Anti-H. pylori EIA). IgA anti-HP in gastric juice was determined by ELISA. HP-positivity included positivity in all methods, and HP-negativity failure to detect HP-infection by all methods used. Of the 20 duodenal ulcer patients, 10 patients (2 female, 8 male; age 26-70 [mean 42] years) had an endoscopically documented duodenal ulcer at an earlier endoscopy with no current ulcer, 10 patients had florid duodenal ulcer disease at the time of examination. Duodenal ulcer patients compared with non-ulcer dyspepsia patients were tended to have higher serum IgG anti-HP (551 +/- 240 vs. 338 +/- 159 U/ml) and significantly higher gastric juice IgA anti-HP (50.0 +/- 7.3 vs. 26.5 +/- 4.3 relative units). Concentrations of both serum IgG anti-HP and gastric juice IgA anti-HP tended to be higher in patients with positive ulcer history but no present ulcer compared with patients with florid ulcer disease (934 +/- 456 vs. 170 +/- 63 U/ml and 60.0 +/- 8.6 vs. 40.8 +/- 10.4 relative units).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Duodenal ulcer disease: a defect in the secretory immune response to Helicobacter pylori?]. 819 Dec 63

In a prospective trial we examined the efficacy and acceptability of a modified triple therapy in H. pylori (HP)-positive patients with recurrent duodenal ulcer disease. Oral administration of amoxicillin for two weeks was substituted for one single injection of intramuscular depot penicillin (benzathine penicillin G). Additionally, patients were given ornidazole 500 mg tid for 14 days and 120 mg colloidal bismuth sub-citrate qid for 28 days. The patients were investigated for H. pylori colonization using a rapid urease test (CLO), histology (H&E-, Giemsa stain), culture (including determination of the minimal inhibitory concentrations for metronidazole, penicillin G and amoxicillin) and H. pylori serology (Cobas Core Anti-H. pylori EIA, F. Hoffmann-La Roche). Control endoscopies using the same methods were performed 1 and 6 months after eradication therapy. The eradication rate was 50% and the ulcer healing rate 90% 1 month after therapy. Ulcers recurred in 2/3 of patients with persistent infection vs 0/5 of HP-eradicated patients after 6 months. Both successfully HP-eradicated patients and patients with treatment failure exhibited comparable decreases in mean serum IgG anti-HP concentration within 2 months. Discrimination between the two groups and hence identification of the eradication success by serology was not possible within a time period of 2 months. After 6 months, serum IgG anti-HP concentrations in non-HP-eradicated patients returned to pre-therapy values, in HP-eradicated patients the concentrations further decreased. The above-described modified triple therapy against HP cannot be recommended as a standard therapy, mainly because of the insufficient eradication effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A trial of modified triple therapy for the eradication of H. pylori in recurrent duodenal ulcer]. 821 Oct 15

Sera from 14 patients with duodenal ulcer and their families were tested for IgG antibodies to Helicobacter pylori. Fourteen serologically negative patients and their families served as controls. Index patients and their family members who were serologically positive were advised to undergo endoscopic biopsy. Gastric biopsy tissues were subjected to HaeIII restriction analysis of nested polymerase chain reaction products of the urease gene. By serology, 28 (49.0%) of 57 in index families and 11 (27.5%) of 40 in control families tested positive. A higher prevalence rate was found in children of index patients (11/31, 35.5%) than in those of control patients (1/18, 5.6%; P < .05). On DNA analysis, 11 patterns were found in 13 patients, and 6 families underwent endoscopy. Children in 5 families exhibited identical patterns to those of their siblings and, in 3 of the 5 families, identical to the pattern of 1 of the parents. These results suggest that parent-to-child transmission and common infection source are probable causes of intrafamilial clustering of H. pylori.
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PMID:Direct DNA amplification and restriction pattern analysis of Helicobacter pylori in patients with duodenal ulcer and their families. 824 43

The sensitivity and specificity of the preformed urease test and of carbolfuchsin-stained smears for the diagnosis of the presence of Helicobacter pylori in gastric mucosa were evaluated before and after antimicrobial treatment. The results obtained by culture were used as the reference point. We studied 41 patients with endoscopically diagnosed duodenal ulcer. Twenty-five of these were treated with furazolidone (100 mg t.i.d.), amoxicillin (500 mg t.i.d.) and metronidazole (250 mg t.i.d.) for 5 days and then with only furazolidone (100 mg t.i.d.) for an additional 25 days. The 16 control patients were treated with cimetidine (800 mg, 4 times a day). The sensitivity of the urease test and of direct smear examination was 100% before treatment and 84.6% and 92.3%, respectively, after treatment. We conclude that the urease test and carbolfuchsin-stained smears, which are highly sensitive for H. pylori diagnosis, present reduced sensitivity when they are employed for the follow-up of patients treated with antimicrobials.
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PMID:Comparison of the urease test and of direct smear examination in the control of treatment of Helicobacter pylori-induced infection. 826 18

A prospective study of infection due to Helicobacter pylori in 104 Southern Appalachian veterans with upper gastrointestinal symptoms revealed a prevalence of 67%. There was no age difference observed between those with and without H pylori. The organism was shown to be present in 12 of 13 patients with duodenal ulcer (92%), 6 of 10 with gastric ulcer (60%), and 52 of 81 with nonulcer dyspepsia (64%). Using culture as standard, the urease test showed a sensitivity of 76% and specificity of 100%, while the biopsy stain had a sensitivity of 97%. The presence of acute inflammation in the antrum and body of the stomach closely correlated with the presence of the organism. Somewhat at variance with previous studies, our study indicated that H pylori in the body mucosa was strongly associated with chronic superficial gastritis with and without acute inflammation. Such a finding may reflect the natural history of infection due to H pylori and the advanced age of our patients.
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PMID:Chronic gastritis associated with infection due to Helicobacter pylori in southern Appalachian veterans with dyspepsia. 827 11

Non-steroidal anti-inflammatory drugs (NSAIDs) and Helicobacter (H pylori) are both associated with an increased risk of peptic ulceration and gastropathy. It is not known, however, if there is an interaction between these two agents, and thus whether or not screening for H pylori before NSAID treatment is of value. The aim of this study was to find out if H pylori potentiates the damaging effects of NSAIDs. Fifty two patients with rheumatoid arthritis requiring longterm NSAID treatment were studied. Dyspeptic symptoms were assessed according to a standardised questionnaire. Gastroscopy was performed after a one week washout period during which NSAIDs were discontinued. Gastric and duodenal mucosal damage was graded endoscopically. H pylori was identified by biopsy urease test and by histological tests. Investigations were repeated after one month's treatment with an NSAID. Patients with H pylori infection (n = 26) had a higher dyspeptic symptom score (p < 0.05). One patient with duodenal ulcer (H pylori +ve) and two with endoscopic gastritis (both H pylori +ve) were excluded from further study. Forty two subjects completed the study. After treatment there was a rise in the gastric damage score both in the H pylori +ve (p = 0.06) and the H pylori -ve (p < 0.005) groups. There was no difference in the extent of increase in grade or the final grade at the end of the treatment period between the H pylori +ve and -ve patients. It is concluded that H pylori infection is associated with increased dyspeptic symptoms in patients receiving NSAIDs but that it does not potentiate NSAID gastropathy.
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PMID:Prevalence of Helicobacter pylori infection and its effect on symptoms and non-steroidal anti-inflammatory drug induced gastrointestinal damage in patients with rheumatoid arthritis. 828 54


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