Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.5.1.5 (urease)
 7,257 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanism of the hypergastrinaemia associated with Helicobacter pylori infection is unknown. It may be an effect of the ammonia produced by the bacterium near the antral epithelial surface. We have examined the effect on serum gastrin of inhibiting H pylori urease activity with acetohydroxamic acid in six duodenal ulcer patients. On day 1 the fasted patients received placebo tablets at 8 am, a peptide meal at 10 am, and a 14C urea breath test at 11.30 am. The next day 750 mg acetohydroxamic acid was administered orally in place of the placebo. The median (range) 30 minute breath test value (dose/mmol CO2 X kg body wt X 100) was 152 (111-335) on day 1, but only 22 (14-95) the next day (p less than 0.03). Further studies performed in one subject confirmed that acetohydroxamic acid lowered the ammonium concentration and raised the urea concentration in gastric juice. The inhibition of urease activity and ammonia production did not result in a fall in the basal gastrin concentration or in the median integrated gastrin response to the peptide meal, which was 78 ng/1.h (range 21-222) on day 1 and 79 ng/1.h (33-207) the next day. Ten days after acetohydroxamic acid, the urea breath test values were similar to those before treatment. This study shows that the raised gastrin concentration in patients with H pylori infection is not directly related to the organism's urease activity. It also shows that temporary suppression of H pylori urease activity does not clear the infection.
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PMID:Effect of inhibition of Helicobacter pylori urease activity by acetohydroxamic acid on serum gastrin in duodenal ulcer subjects. 188 67

It has been proposed that the hypergastrinaemia in subjects with Helicobacter pylori infection is caused by the action of the ammonia produced by the organism's urease activity on the antral G cells. To investigate this hypothesis we examined the effect on plasma gastrin of increasing the bacterium's ammonia production by infusing urea intragastrically to eight H pylori positive duodenal ulcer patients. After a 60 minute control intragastric infusion of dextrose solution at 2 ml/minute, a similar infusion containing urea (50 mmol/l) was continued for four hours. During the urea infusion, the median gastric juice urea concentration rose from 1.1 mmol/l (range 0.3-1.6) to 15.5 mmol/l (range 7.9-21.3) and this resulted in an increase in the ammonium concentration from 2.3 mmol/l (range 1.3-5.9) to 6.1 mmol/l (range 4.2-11.9) (p less than 0.01). This appreciable rise in ammonia production did not result in any change in the plasma gastrin concentration. The experiment was repeated one month after eradication of H pylori, at which time the median basal gastrin was 20 ng/l (range 15-25), significantly less than the value before eradication (30 ng/l range 15-60) (p less than 0.05). On this occasion, the gastric juice ammonium concentration was considerably reduced at 0.4 mmol/l (range 0.1-0.9) and the urea infusion did not raise the ammonium concentration or change the plasma gastrin concentration. In conclusion, augmenting H pylori ammonia production does not cause any early change in plasma gastrin.
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PMID:Effect of increasing Helicobacter pylori ammonia production by urea infusion on plasma gastrin concentrations. 199 33

Recent studies have shown that the exaggerated meal-stimulated gastrin release in patients with duodenal ulcer abates after eradication of Helicobacter pylori infection. Bombesin-stimulated gastrin release was compared in 11 H. pylori-infected patients with chronic duodenal ulcer and 8 uninfected healthy volunteers both before and after therapy to eradicate H. pylori. Bombesin infusion significantly increased the gastrin release both in control subjects and in patients with duodenal ulcer. Antimicrobial therapy (bismuth, tetracycline, and metronidazole) to eradicate the H. pylori infection was associated with a significant reduction in bombesin-stimulated gastrin release in patients with duodenal ulcer (from 116.9 +/- 19 pg/mL to 69.5 +/- 7 pg/mL following 50 pmol.kg-1.h-1 bombesin; and from 158 +/- 29 to 83.4 +/- 10 following 200 pmol.kg-1.h-1 bombesin: P = 0.01 for each). Antimicrobial therapy had no effect on gastrin release in uninfected volunteers, thus excluding a nonspecific effect of antimicrobial therapy on antral G-cell function. Serum gastrin was also not increased by feeding 500 mg of urea to 5 H. pylori-infected volunteers. This suggests that access of hydrogen ion to the pH-sensitive sites governing gastrin release by mucosal ammonia produced by H. pylori urease is not a critical factor. These data suggest that exaggerated gastrin release present in patients with duodenal ulcer disease is secondary to H. pylori infection.
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PMID:Helicobacter pylori-associated exaggerated gastrin release in duodenal ulcer patients. The effect of bombesin infusion and urea ingestion. 201 63

Helicobacter mustelae has been cultured from the stomachs of ferrets with chronic gastritis; the lesions in the stomach have many of the same histological features seen in H. pylori gastritis in humans. To determine whether H. mustelae-negative ferrets with normal gastric mucosa were susceptible to colonization and whether gastritis developed after infection, four H. mustelae-negative ferrets treated with cimetidine were inoculated orally on two successive days with 3 ml (1.5 x 10(8) CFU) of H. mustelae; eight age-matched H. mustelae-negative ferrets served as controls. All four ferrets became colonized; H. mustelae persisted through week 24 of the study, as determined by positive gastric culture, tissue urease, and Warthin-Starry staining of gastric tissue. Superficial gastritis developed in the oxyntic gastric mucosa, and a full-thickness gastritis, composed primarily of lymphocytes and plasma cells plus small numbers of neutrophils and eosinophils, was present in the antrum. The inflammation was accompanied by an elevation of immunoglobulin G antibody to H. mustelae. At 4 weeks post-inoculation, the four infected (experimental) ferrets developed an elevated gastric pH (4.0 to 5.2) for 2 weeks. The eight control ferrets did not have gastritis; H. mustelae could not be demonstrated in gastric tissue via culture, nor was there an immune response to the bacteria. In ferrets, H. mustelae readily colonizes the stomach and produces a gastritis, a significant immune response, and, like H. pylori infection in humans, a transient elevated gastric pH after Helicobacter infection.
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PMID:Helicobacter mustelae-induced gastritis and elevated gastric pH in the ferret (Mustela putorius furo). 203 49

Twenty three children with coexistent duodenal ulcer and Helicobacter pylori infection were treated with either two weeks of amoxycillin (25 mg/kg/day) in addition to six weeks of cimetidine, or cimetidine alone. Endoscopy with antral and duodenal biopsies for urease test, microaerophilic culture, and histological studies were performed at entry, six weeks, 12 weeks, and at six months. Children with persistent H pylori infection at six weeks were given a further two weeks' course of amoxycillin. H pylori persisted in all children not receiving amoxycillin treatment but cleared in six of the 13 children (46%) treated with amoxycillin. With failure of H pylori clearance at six months, only two out of six (33%) ulcers had healed and 50% of patients had experienced ulcer recurrence. In contrast, when H pylori remained cleared all ulcers healed and no ulcer recurred. Persistent H pylori infection was associated with persistent gastritis and duodenitis despite endoscopic evidence of ulcer healing. Detection and eradication of H pylori deserves particular attention in the routine management of duodenal ulceration in children.
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PMID:Helicobacter pylori and associated duodenal ulcer. 224 31

The biopsy urease test is a simple and rapid method for the diagnosis of Helicobacter pylori infection; results are obtained within 4 h to 24 h. Various modifications of the media used in this test have been tried, to improve the accuracy and speed of the test. We compared the yield obtained with two media: the standard Christensen's urea medium and a modified plain urea medium (without the nutrients glucose and peptone); the result was read upto 1 h. In the first 53 cases, culture was obtained when either of the media gave a negative result. There was no difference in false positives in the two media, while there were more false negatives with the plain urea medium (4) compared to the Christensen's medium (1). In the latter 69 patients, we determined the accuracy of the two media by obtaining culture in all cases. The Christensen's medium had a sensitivity of 100% and a specificity of 92.1%, while the plain urea medium had a sensitivity of 96.7% and a specificity of 92.1%. The speed of reaction in both media was similar. We conclude that the Christensen's urea medium gives accurate results even when read at 1 h; the plain urea medium gives similar results.
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PMID:Evaluation of a modified medium for the one hour urease test for Helicobacter pylori infection. 237 33

Numerous reports have established the association of Helicobacter pylori and peptic ulcer disease in adults. Recently, this association has also been demonstrated in children. We investigated 14 children and adolescents with recurrent abdominal pain. In six patients, endoscopy revealed gastritis and Helicobacter pylori was identified. Giemsa stain was more sensitive than culture or urease testing in identifying the bacteria. In four of the six, a nodular appearance of the antral mucosa was observed. The histological examination suggests lymphoid hyperplasia as the cause of the nodularity. All of the patients became symptomless after combined treatment with amoxicillin and bismuth subsalicylate. We conclude that nodular gastritis is a peculiar type of gastritis in children. It is frequently found in association with Helicobacter pylori infection.
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PMID:Nodular gastritis and Helicobacter pylori. 205 Dec 85

Chronic active type B gastritis is invariably the result of Helicobacter pylori infection and is an important factor in duodenal ulcer disease. The actions of mediators produced (a protein factor, a lipid soluble "pore-forming factor" and urease) or induced (immune/inflammatory cell mediators) by this bacterium on the control of gastric acid secretion are currently being investigated. These studies are reviewed in light of our current knowledge of the physiological control of gastric acid secretion.
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PMID:Inflammation, acid and ulcers. 750 22

Patients with recurrent upper abdominal complaints and without peptic ulcer or definite evidence of organic disease have been labelled as suffering from nonulcer dyspepsia and included in the study. A total of 125 patients were studied and upper gastrointestinal endoscopy performed. Histology, urease rapid test and ELISA serology were done in order to detect Helicobacter pylori infection. Age groups were done. The most frequent endoscopic and histological finding was chronic gastritis in all age groups of patients. In patients under 30 years old, the highest rate of normal endoscopy was found. Chronic gastritis was associated with Helicobacter pylori infection in 89.8% of all patients. The highest rate of chronic gastritis non associated with Helicobacter pylori infection was found in the age group of patients younger than 30 years old. Other factors as biliary reflux, gastroduodenal dismotility, decreased pain tolerance or stress have been proposed to be the etiology of chronic gastritis in young patients.
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PMID:[Chronic gastritis and Helicobacter pylori in patients with non-ulcerous dyspepsia. Role and significance of age]. 757 11

The urea breath test exploits the urease enzyme of Helicobacter pylori. The hydrolysis of labelled urea releases labelled carbon dioxide that is excreted in the breath. Distribution of urea throughout the stomach prevents sampling errors and allows for semiquantitative assessment of the extent of Helicobacter pylori infection. The urea breath test is very specific and sensitive and can be proposed as the method of choice for detecting Helicobacter pylori infection in ulcer patients before and after eradicating treatment as well as in epidemiological studies.
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PMID:The urea breath test: a non-invasive clinical tool for detecting Helicobacter pylori infection. 757 92


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