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)

This study examined a possible aetiological agent, namely, Helicobacter pylori, in perforated peptic ulcer disease and its relationship to persisting ulcer. Twenty-nine patients with perforated peptic ulcer underwent simple closure of the perforation at laparotomy. A 13C urea breath test carried out on the eighth day after operation was positive in 24 patients. Fourteen of 17 patients who underwent upper gastrointestinal endoscopy 6 weeks after discharge from hospital had a positive 13C urea breath test. The biopsy urease test performed on mucosal samples taken at endoscopy was positive in 12 of these 14 patients, indicating continuing active infection with H. pylori. Seven patients with positive 13C urea breath and biopsy urease tests had persisting duodenal ulceration. None of the three patients with a negative 13C urea breath test had evidence of duodenal ulceration at endoscopy. The association between a high rate of duodenal ulcer persistence and a high incidence of H. pylori infection suggests that antibiotic therapy to eradicate this microorganism should be given to all patients with perforated peptic ulcer disease.
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PMID:Helicobacter pylori infection in perforated peptic ulcer disease. 779 9

The authors report the results of the detection of Helicobacter Pylori (HP) in gastric mucosa by the urease test, in 244 patients between January 1989 and August 1991. The overall prevalence of HP was 38.1%. It was 19.5% in patients with normal upper gastrointestinal endoscopy (UE), 61% in duodenal ulcer (p < 0.001) and 68.7% in congestive antritis (p < 0.001), significantly higher than in controls. There was no significant difference between controls and patients with erosive antritis or healed duodenal ulcers. The prevalence of HP rises with age in all patients and in those with lesions at UE but not in those with normal UE. A rise of this prevalence seems to exist in the months of June and December. The authors conclude by pointing out the rise of the overall prevalence of HP in congestive antritis compared with erosive antritis, the similarity of prevalence in normal subjects and those with healed ulcer and the lack of influence of age on this prevalence in subjects with normal UE. These conclusions are in need of confirmation by further studies on much more longer series.
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PMID:[Detection of Helicobacter pylori by the urease test in 244 patients]. 779 11

We studied the prevalence of Helicobacter pylori in Sudanese subjects with gastroduodenal inflammation. H. pylori was looked for in biopsy specimens taken from the antrum by two methods: rapid urease test [Campylobacter-like organism (CLO) test] and culture using Skirrow's selective supplement. One hundred subjects were studied. H. pylori was found in 80% of patients with gastritis, 56% of patients with duodenal ulcer, 60% of patients with duodenitis and 16% of normal control subjects. It was neither detected in patients with gastric ulcer, nor in patients with oesophagitis or in those with oesophageal varices due to schistosomiasis, when using culture. However, it was found in 50% of patients with oesophagitis, when using CLO test.
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PMID:Detection of Helicobacter pylori in endoscopic biopsies in Sudan. 780 58

One hundred and two consecutive patients undergoing upper gastrointestinal endoscopy were tested for H. pylori by a rapid urease test, using antral biopsy specimens. There were 60 men (mean age 54 yrs) and 42 women (mean age 49 yrs). Fifty-six patients (55%) were positive for H. pylori. Of male patients, 36 (60%) and of female patients, 20 (48%) tested positive. Sixty-eight per cent of patients with antral gastritis, 65% with duodenal ulcer and 60% with gastric ulcer had H. pylori. Thirty-nine patients (70%) positive for H. pylori were from major urban areas, and 17 (30%) were from rural areas of Jamaica. In patients without H. pylori, 61% and 39% were from urban and rural areas, respectively. Forty-four patients (79%) with H. pylori and 40 (87%) without H. pylori had piped water in their homes. Ninety-three per cent of all patients had electricity and 88% had refrigeration. There was no difference between patients positive or negative for H. pylori with regard to the use of alcohol, marijuana or tobacco. There was also no difference between both groups in exposure to domestic animals in the home environment. H. pylori is associated with antral gastritis and peptic ulcer disease in Jamaican patients. There are no specific environmental or social factors that seem to predispose to infection.
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PMID:Helicobacter pylori in patients undergoing upper endoscopy in Jamaica. 781 42

Among the patients subjected to esophoagogastroduodenoscopy because of different clinical indications, 108 were examined for the presence of Helicobacter pylori in the antral gastric mucosa. Microbiological analysis of the antral gastric mucosa biopsies were conducted by direct microscopy, the urease test and by growing in nutritious media. Positive findings were recorded in 38 (86.36%) patients with endoscopically diagnosed chronic gastritis, 29 (80.56%) patients with duodenal ulcer and 19 (67.86%) patients with ventricular ulcer. The majority of the positive findings were recorded by direct microscopy--86 (79.63%) while the bacterial culture was positive in 66 (61.11%) cases.
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PMID:[Helicobacter pylori in patients with diseases of the upper part of the gastrointestinal tract]. 786 44

Helicobacter pylori associated duodenal ulcers occur in patches of gastric metaplasia. The pathogenesis of gastric metaplasia is unclear, but it has been produced in experimental animals by acute injury and has been shown to be present to a greater extent of H pylori positive subjects. This study aimed to discover if gastric metaplasia regressed with eradication of H pylori or healing of duodenal ulcers, or both. Thirty two duodenal ulcer patients with H pylori infection confirmed by biopsy urease test and by antral histological examination were studied. Patients were treated with triple therapy (deNol 240 mg twice daily, amoxycillin 500 mg three times daily, and metronidazole 400 mg three times daily) for two weeks after the first endoscopy and were subsequently re-endoscoped. Three duodenal bulb biopsy specimens were obtained per patient at each endoscopy. Biopsy sections were stained with haematoxylin and eosin to determine the severity of duodenitis, and with diastase periodic acid-Schiff/alcian blue to assess the extent of gastric metaplasia. Slides were assessed by two histopathologists unaware of treatment status. H pylori was eradicated in 63% of subjects and all ulcers were healed at follow up. The median extent of gastric metaplasia at the start of treatment and 6-18 months (median 10) after treatment was compared in the two groups. Gastric metaplasia declined in eradicators from 16% to 8% (p < 0.05) while in non-eradicators there was no significant change (25% initially and at follow up). A positive relation between extent of gastric metaplasia and duodenal inflammation score was present before treatment (r(s) = 0.74, p < 0.001) and was unchanged after treatment in the non-eradicator group (r(s) = 0.89, p < 0.001). In the eradicator group, however, the inflammation score had significantly declined (p < 0.02) and the close relation with gastric metaplasia was no longer present. These results suggest that H pylori itself is at least in part responsible for producing gastric metaplasia of the duodenum.
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PMID:Effect of Helicobacter pylori eradication on gastric metaplasia of the duodenum. 759 Apr 50

The aim of this study was twofold: first, to investigate the effectiveness of a standard triple therapy (tripotassium dicitrato bismuthate, 125 mg q.i.d., tetracycline hydrochloride 500 mg q.i.d., and metronidazole 500 mg t.i.d.) in eradicating Helicobacter pylori in patients with duodenal ulcer successfully healed with omeprazole or ranitidine; second, to examine the influence of the eradication on duodenal ulcer recurrence rate after 12 months. Two hundred forty-five consecutive H. pylori-positive patients with healed duodenal ulcer either with omeprazole (20 mg/day, 126 patients) or with ranitidine (150 mg b.i.d., 119 patients) given at random, began triple therapy for 15 days. H. pylori eradication was looked for 4-5 weeks later by culture of biopsy material, hematoxylin-eosin stain, and rapid urease test. H. pylori-eradicated patients were followed up for 12 months. Endoscopy was carried out at the end of the follow-up or whenever symptoms appeared. Five patients (2.0%) withdrew because of triple-therapy-related side effects. The eradication rate was 92% (220 of 240 patients); no difference was found between those healed with omeprazole (93%, 114 of 123 patients) or ranitidine (91%, 106 of 117 patients). Of 220 successfully treated patients, 132 completed the 12-month follow-up. The duodenal ulcer recurrence rate was 4% (5 of 132 patients); 3% (2 of 70) in the omeprazole group and 5% (3 of 62) in the ranitidine group healed. All the recurrences were asymptomatic. H. pylori recurrence rate was 11% (14 of 132 patients); no difference was found between patients healed with omeprazole (10%, 7 of 70 patients) or with ranitidine (11%, 7 of 62 patients). All the recurrent duodenal ulcers occurred in H. pylori-positive patients (36%, 5 of 14 patients). Standard triple therapy after duodenal ulcer healing with omeprazole or ranitidine eradicates H. pylori in comparable high rates. Side effects were mild and dropouts were only 2%. Ulcer recurrence rate 12 months after eradication was low and comparable between those healed with omeprazole or ranitidine.
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PMID:Triple therapy eradicated H. pylori equally in patients pretreated with omeprazole or ranitidine. A 12-month follow-up. 788 69

In a prospective study 27 patients (13 women, 14 men; mean age 62 [45-83] years) with Helicobacter (H.) pylori associated disease received over 7 days pantoprazole (40 mg twice daily), clarithromycin (500 mg twice daily) and metronidazole (500 mg twice daily). Six patients had gastric ulcer, 4 duodenal ulcer, 4 erosive gastritis, 6 erosive duodenitis and 7 had H. pylori-positive functional dyspepsia. Pre-treatment oesophago-gastro-duodenoscopy was combined in 4 patients with antral and in 4 others with body-of-stomach biopsies to demonstrate H, pylori (urease test, specific culture and histology). The H. pylori status was checked with the 13C-urea breath test 4 weeks after the end of treatment. In addition, 9 patients with peptic ulcer were examined endoscopically at least 2 weeks after onset of the treatment to check for any healing of the ulcers, 25 of the patients completed the study according to the protocol. The H. pylori eradication rate was 100% (25 of 25 patients), while the "intention to treat" analysis gave a rate of 92.6% (25 of the 27 patients). The peptic ulcers were found to be healed in all 9 patients who had been endoscoped. One woman developed a reversible stomatitis, but the drug treatment did not have to be stopped. -These findings indicate that short-term triple treatment in the described manner is efficacious in curing H. pylori infection and any peptic ulcer. It is thus a highly promising treatment of H. pylori-associated diseases.
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PMID:[Short-term triple therapy with pantoprazole, clarithromycin and metronidazole for the healing of Helicobacter pylori infection]. 788 16

Omeprazole is a powerful inhibitor of gastric acid and may suppress Helicobacter pylori by effecting the pKa of H pylori urease, by altering the pattern of infection, or by promoting overgrowth of other bacteria. At routine endoscopy H pylori was detected by histology and culture before and after four weeks' treatment with omeprazole, 40 mg each morning. A 13C-urea breath test was also done at t = 0, 2, 4, and 6 weeks. Thirty nine patients with duodenal ulcer (n = 25) or reflux oesophagitis (n = 14) were studied, of whom 29 of 39 had H pylori infection. During omeprazole treatment, 13C-urea breath test values fell significantly--mean (SEM) values before treatment and at four weeks were 23.0 (2.1) and 15.5 (2.7) per mil respectively, p < 0.001. Before treatment H pylori was seen in 28 of 29 antral, 29 of 29 corpus, and 28 of 29 fundic biopsy specimens. After four weeks of omeprazole treatment, the histological density of H pylori in the antrum and corpus was reduced (p < 0.001), while that in the fundus was increased. The migration of H pylori from the antrum to the fundus was associated with a corresponding decrease in the activity of antral gastritis. H pylori was not seen in antral biopsy specimens from 12 of 29 patients whose median excess delta 13CO2 excretion fell from 23.0 to 9.9 per mil. In the body mucosa, 26 of 29 specimens were still positive for H pylori and there was no significant change in the gastritis type. Two weeks after finishing treatment, the mean (SEM) excess delta 13CO2 excretion returned to levels before treatment. Omeprazole decreases antral H pylori colonisation but increases that in the fundus. The changes in the intragastric distribution of the organism are associated with concomitant changes in the activity of gastritis and are matched by a progressive fall in the excretion of delta 13CO2.
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PMID:Changes in the intragastric distribution of Helicobacter pylori during treatment with omeprazole. 789 Feb 14

Helicobacter pylori is a microaerophilic bacterium initially found in the gastric antrum of patients with peptic ulcer disease. As a result, H. pylori is now believed to have a pathophysiologic role in gastritis as well as in peptic ulcer disease. Several recent studies showed that it may be associated with duodenal ulcer relapse and that eradication therapy using antibiotics may significantly decrease the ulcer recurrence rate in duodenal ulcer patients. Moreover, epidemiological studies suggest that it may increase the relative risk of carcinoma in the stomach and preliminary studies seem to indicate that some low-grade lymphoma in the stomach may regress after H. pylori eradication. Although the mechanisms by which H. pylori induces mucosal injury and/or neoplasm is not clearly understood, several modifications in gastric functions have been reported. The most specific way of detecting H. pylori in tissue is a combination of culture and histologic staining of mucosal biopsy specimens obtained by endoscopy. Rapid urease test, cytology and PCR procedures performed on biopsies may give rapid, sensitive and specific results. Breath test using 13C- or 14C-radiolabelled urea and serology tests are of particular importance when H. pylori diagnosis is needed via no invasive procedures. Helicobacter pylori is supposed to interact with G and D cells. Gastrin and somatostatin are synthetized and released from antral G and gastric D cells respectively. The gastric D cells are in close contact with either G and parietal cells. Gastrin stimulates gastric acid secretion and epithelial gastric cell proliferation (parietal and EC-L cells) while somatostatin inhibits these effects. Chronic gastritis is associated with fundic duodenal ulcer disease. In this situation, basal gastrin and meal- or bombesin-stimulated gastrin in the serum (especially gastrin G17) have been found to be higher in H. pylori positive than in negative patients. Moreover, gastrin decreases up to normal levels after eradication of H. pylori. The long term effect of a such hypergastrinemia is not so far established. The mechanism underlaying hormonal modification is poorly understood. Since no G/D cell ratio modification could be found after H. pylori eradication while the amount of somatostatin increases, one would suggest functional alteration of either G or D cells in the H. pylori-related chronic gastritis. The role of inflammatory mediators on the gastrin release and the processing of progastrin induced by the bacterium need further investigations.
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PMID:[Helicobacter pylori, a rediscovered bacterium. Implication in gastroduodenal diseases]. 789 50


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