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)

We defined optimal Helicobacter pylori (Hp) treatment as Hp eradication rate about 90%, well-tolerated with few side-effects. Two centers carried out randomized trials including 90 patients (74% men, 26% women, ages ranging from 18 to 65, mean age 42 +/- 8) with active duodenal ulcers (DU). Patients were treated with the combination of Omeprazole (O) 20 mg bd + Clarithromycin (C) 250 mg bd + Tinidazole (T) (500 mg bd) or with Lansoprazole (L) 15 mg bd + Amoxicillin (A) 750 mg bd + Metronidazole (M) 500 mg bd administered for one week. The DU healing rate was evaluated by endoscopy and the Hp status by rapid urease CLO-test and 14C-urea breath test (UBT). The healing rate of the DU in a group treated with the combination of O + C + T was 91% and in group treated with L + A + M was 93%. The eradication of Hp in group O + C + T and L + A + M averaged 91% and 87%, respectively. There was no statistically significant difference in the DU healing rate and the Hp eradication rate between these two groups. Both treatments were accompanied by a marked rise in the basal and postprandial plasma gastrin levels and the rise in the intragastric pH but these alterations returned to the pre-treatment values 4 weeks after the termination of the therapy. Both treatments were well tolerated and the only side effect was the taste disturbance observed in few patents treated with O + C + T. None of patients discontinued the treatment because of the adverse events. We conclude that one week treatment using O + C + T or L + A + M are highly and equally effective in the healing of DU and in the eradication of Hp.
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PMID:One week treatment with omeprazole, clarithromycin and tinidazole or lansoprazole, amoxicillin and metronidazole for cure of Helicobacter pylori infection in duodenal ulcer patients. 877 3

The aim of the present study was to examine the efficacy and safety of combination therapy with amoxicillin (AMPC), lansoprazole, and plaunotol for the eradication of H. pylori in dialysis patients. The subjects consisted of 15 dialysis patients (10 men and 5 women, mean age of 56 +/- 2.4 years) in whom H. pylori was found in the stomach. H. pylori status was evaluated by histology, culture and rapid urease test with biopsy specimens of the gastric mucosa. The patients were treated with AMPC 500 mg once a day for 3 weeks, lansoprazole 30 mg once a day for 8 weeks and plaunotol 80 mg three times a day for 24 weeks. In addition, the concentrations of serum gastrin and gastric juice ammonia were measured. Fourteen patients completed the treatment schedule, while one discontinued treatment because of nausea and diarrhea. Among the 14 patients, H. pylori was eradicated in 11 without any side effects (eradication rate 78.6%). Concentrations of gastric juice ammonia and serum gastrin were reduced significantly in patients who became H. pylori-negative. The present study indicates that combination therapy with AMPC, lansoprazole and plaunotol is safe and efficient for the eradication of H. pylori in dialysis patients. The results also suggested that elevated concentrations of gastric juice ammonia and serum gastrin in dialysis patients can be attributed, at least in part, to H. pylori infection.
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PMID:[Eradication of Helicobacter pylori in patients with end-stage renal disease undergoing dialysis treatment]. 882 54

Infection with Helicobacter pylori (H. pylori) is now recognized as a major factor in the pathogenesis of gastric disease, and the successful therapy regimens require a combination of H2 blockers with gastroprotective and antimicrobial agents. Ebrotidine (N-[(E)-[[2-[[[2-[(diaminomethylene) amino]-4-thiazolyl] methyl]thio]ethyl]amino]methylene]-4-bromo-benzenesulfonamide, CAS 100981-43-9, FI-3542) is the only drug combining acid-suppressant activity with remarkable gastroprotective and anti-H. pylori properties. The drug not only displays a potent anti-H. pylori activity alone, but also exerts a strong potentiating effect on the efficacy of antimicrobial agents commonly used for H. pylori eradication, and the successful ulcer therapy with ebrotidine induces a significant (4-fold) increase in the H. pylori aggregation titer of gastric mucin. Moreover, the drug exhibits a strong inhibitory effect on H. pylori urease activity, the extent of which exceeds that of ranitidine, omeprazole and lansoprazole. Ebrotidine has also been demonstrated to exert a potent inhibitory action on the enzymatic activities directed towards mucus perimeter of gastric mucosal defense, causing a marked inhibition of H. pylori protease, lipase and phospholipase A2 activities. Another important property of ebrotidine is its ability to efficiently counteract the disruptive effects of H. pylori lipopolysaccharide on the integrity of gastric epithelium. This includes countering the interference by the lipopolysaccharide in mucosal integrin receptor interaction with proteins of extracellular matrix and the reversal of H. pylori disruptive effect on the binding of mucin to its gastric epithelial receptor. Furthermore, most recent data indicate that ebrotidine has the ability to reverse the impairment caused by H. pylori in feedback inhibition of gastrin release by somatostatin. This activity of ebrotidine apparently stems from the drug's ability to counter the untoward effect of H. pylori on the binding of somatostatin to its specific receptor on the gastric mucosal G-cells. The unique combination of acid suppressant, gastroprotective and anti-H. pylori activities makes ebrotidine a drug of choice in the treatment of gastric disease caused by H. pylori.
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PMID:Anti-Helicobacter pylori activities of ebrotidine. A review of biochemical and animal experimental studies and data. 920 47

Gastric mucosa is exposed to various aggressive factors such as stress, ulcerogenic drugs including acetyl-salicylic acid(ASA)-like agents, ethanol, bacteria, particularly Helicobacter pylori (Hp), and various endogenous irritants such as acid-pepsin secretion and bile salts. The maintenance of the mucosal barrier depends upon the activation of the pre-epithelial (mucus-alkali secretion), epithelial (surface-active phospholipids and rapid mucosal restitution) and post-epithelial (mucosal microcirculation, sensory nerves and mast cells) components of mucosal defense. Ebrotidine (N-[(E)-[[2-[[[2-[(diaminomethylene)amino]- 4-thiazolyl]methyl]thio]ethyl]amino]methylene]-4-bromo-benzenesulfonamid e, CAS 100981-43-9, FI-3542) is the first of a new generation of H2-receptor antagonists with both antisecretory and cytoprotective activities. Its inhibitory action is similar to that of ranitidine and approximately tenfold greater than cimetidine, and is accompanied by a small and transient increase in plasma gastrin levels. In contrast to ranitidine and other H2-receptor antagonists, ebrotidine exerts a unique cytoprotection against injury by various ulcerogens such as ethanol, ammonia, lipopolysaccharides (LPS), stress and ASA or acidified taurocholate. The mechanism of this protection by ebrotidine is not clear, but it has been shown to stimulate mucus secretion, to increase the quality of adherent mucus gel and to increase gastric mucosal blood flow (GBF), possibly due to enhanced mucosal formation of prostaglandin E2 (PGE2) and nitric oxide (NO). The cytoprotective effects of ebrotidine were observed in rats and confirmed also in humans with gastric lesions induced by ethanol or ASA. Ebrotidine also exerts anti-Helicobacter pylori (Hp) effects by interfering with surface receptors of epithelial cells and inhibiting urease, protease and lipase activity, and by counteracting the noxious effects of Hp-related substances such as ammonia and lipopoly-saccharides (LPS).
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PMID:Studies on the cytoprotective and antisecretory activity of ebrotidine. A review. 920 69

The aims of this study in 50 patients with H. pylori infection and duodenal ulcer were to examine the effect of eradication therapy on the serum levels of gastrin, pepsinogen I, and pepsinogen II and to investigate whether monitoring of the serum changes in these peptides after treatment could predict patient outcome. H. pylori status was assessed at entry and one and six months after therapy by culturing and microscopic analysis of the gastric mucosa and by [14C]urea breath test. Significant decreases were observed in the serum levels of gastrin (-11.4 +/- 3%), pepsinogen I (-28.9 +/- 4%), and pepsinogen II (-40.4 +/- 3%) in the 45 patients whose infection was eradicated, but not in the patients without eradication. Serum values of these peptides were unchanged in an additional group of 10 patients that only received omeprazol, none of whom had H. pylori eradicated. The best cutoff point of the percentage of each peptide to predict patient outcome was 10% for gastrin and pepsinogen I, and 15% for pepsinogen II. A pepsinogen II decrease > 15% resulted in the best marker of H. pylori clearance, accurately identifying patient outcome 86.6% of the time, whereas the diagnostic accuracy of gastrin and pepsinogen I was 61.7% and 76.6%, respectively. Significant correlations were found between the bacterial load assessed by histology with the serum concentrations of pepsinogen I and II and with the urease activity as measured by the amount of 14CO2 excreted. In conclusion, eradication of H. pylori infection is followed by a significant drop in serum levels of gastrin, pepsinogen I, and pepsinogen II. Changes in the latter are the most uniform and may be used as an indirect tool to predict treatment outcome.
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PMID:Changes in gastrin and serum pepsinogens in monitoring of Helicobacter pylori response to therapy. 928 42

To clarify the prevalence of Helicobacter pylori infection in enlarged fold gastritis, serum immunoglobulin (Ig) G antibody to H pylori was determined in 19 patients with severely enlarged gastric body folds (the widest fold greater than 10 mm on the radiograph), 55 patients with moderately enlarged folds (6 to 10 mm) and 44 control subjects (5 mm or less). The prevalence of serum IgG antibody to H pylori in the severe (100%) and moderate groups (100%) was significantly higher than that in controls (34.1%) (P < 0.01). There were significant differences among the three groups in serum gastrin, pepsinogen I and pepsinogen II levels (severe had the highest levels, followed by moderate and then controls, P < 0.001). H pylori colonization in the gastric mucosa was confirmed by culture, urease test or both, and inflammation by hematoxylin and eosin stain in the 25 H pylori seropositive patients who underwent endoscopy and biopsy. Results suggest that H pylori infection is highly prevalent in enlarged fold gastritis. Further studies on enlarged fold gastritis and H pylori infection are needed.
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PMID:High prevalence of serum immunoglobulin G antibody to Helicobacter pylori and raised serum gastrin and pepsinogen levels in enlarged fold gastritis. 928 79

The mechanism by which Helicobacter pylori (Hp) predisposes to duodenal and gastric ulcers remains still unclear. It is possible that Hp infection impaires gastric secretion. Evaluation of gastric acid and mucus secretion before and after Hp eradication would let to estimate the influence of Hp infection on gastric secretion. To evaluate the effect of Hp infection on gastric acid and gastric mucous secretion before and one year after Hp eradication. We examined 28 Hp positive peptic ulcer disease patients (10-gastric ulcer GU, 18-duodenal ulcer DU) before and one year after antibacterial treatment. Gastric acid output was examined basely (BAO) and in response to pentagastrin (6 micrograms/kg) (MAO) using Kay's standard method. Some components of gastric mucus as fucose, galactose, hexosamines and sialic acid were measured using calorimetric methods basaly and after pentagastrin stimulation. Plasma gastrin concentration was measured in 20 patients (6-GU, 14-DU) by radioimmunoassay before and one year after eradication. Hp status was determined by rapid urease test (CLO) and histology (Giemsa stain). One year after Hp successful eradication gastric acid secretion was significantly reduced-BAO: 3,31 vs 1,474 mmol/h; MAO: 19,63 vs 14,85 mmol/h, p < 0.05. Plasma gastrin concentration decreased significantly from 9,783 to 6,017 pmol/I, p < 0.05. In patients with ineffective eradication we did not observe any significant changes in gastric acid secretion. An evident, but not statistically significant, decrease of sialic acid output in eradicated patients was noted. The study has shown the significant influence of Hp infection on gastric acid secretion. Those results support the hypothesis that increased gastric acid secretion may be one of the pathogenic mechanism of Hp infection inducing mucosal damage.
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PMID:Helicobacter pylori infection and gastric secretion in duodenal and gastric ulcer patients--the effect of eradication after one year. 937 18

There are no studies of changes in immunoglobulin G (IgG) titers to Helicobacter pylori, serum pepsinogen, and gastrin in patients with H. pylori-positive gastric ulcers. We investigated the effect of therapy for H. pylori-positive gastric ulcer on IgG titers to H. pylori, serum pepsinogen I and II, and gastrin. Thirty-six patients with H. pylori-positive gastric ulcer were treated with lansorazole and antibiotics for 2 weeks. Serum pepsinogen I and II concentrations, serum gastrin, and IgG titers to H. pylori were measured before treatment and then at 4 and 12 weeks after stopping the treatment. The presence or eradication of H. pylori was determined using the rapid urease test and by histologic H. pylori staining. For 19 patients in whom H. pylori had been successfully eradicated, the pepsinogen I/II ratio increased, pepsinogen II levels decreased, and the anti-H. pylori IgG decreased compared with the results from before therapy and with those from 4 and 12 weeks after therapy. Gastrin levels decreased compared with pretreatment results and those from 4 weeks after the end of treatment. In 17 patients in whom the therapy failed to eradicate H. pylori infection, there were no sequential significant changes in the pepsinogen I/II ratio or in the levels of pepsinogen I, pepsinogen II, anti-H. pylori IgG, and gastrin. A decrease in the serum levels of the IgG antibody to H. pylori and gastrin and also an increase in the pepsinogen I/II ratio could be used as predictors for the eradication of H. pylori infection in gastric ulcer.
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PMID:Changes in serum pepsinogen, gastrin, and immunoglobulin G antibody titers in helicobacter pylori-positive gastric ulcer after eradication of infection. 941 11

The peptic ulcer of gastric tube using for esophageal reconstruction is rare. We report herein five cases of peptic ulcer of gastric tube used for esophageal reconstruction after esophagectomy for esophageal carcinoma. The reconstructive route, in all cases, was posterior mediastinum. In one case, 10 days after esophagectomy, he had high grade fever and pneumonia of right lower lobe of lung. Endoscopic examination revealed a deep ulcerative lesion on anterior wall of gastric tube and fistula formation on membranous part of trachea. The partial resection of gastric tube was performed for closing to tracheo-gastro fistula. In other four cases, the location of ulcer was middle or lower third of gastric tube. One had multiple peptic ulcer and other had single. Two cases of four underwent post irradiation therapy. One case of then, the Helicobacter infection detected using by rapid urease test and histological examination. We analyzed of Helicobacter pylori infection and serum gastrin level of gastric tube in outpatients who have used gastric tube for esophageal reconstruction after radical esophagectomy. Helicobacter pylori infection was positive at 56% (9/16) of all patients. The serum gastrin level of patients who was positive of Helicobacter pylori infection is not significantly higher than that of patients who was negative. We consider that post operative irradiation therapy and Helicobacter infection might play in development of peptic ulcer of gastric tube.
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PMID:[Five cases of peptic ulcer of gastric tube after radical esophagectomy for esophageal carcinoma and analysis of Helicobacter pylori infection at gastric tube]. 945 13

Helicobacter pylori infection in humans has been shown to be associated with changes in gastric physiology, including exaggerated basal and meal-stimulated gastrin levels. This has been suggested to be due to the direct effects of the bacterium through inflammation and its urease enzyme. The gastric bacteria Helicobacter felis and Helicobacter heilmannii colonize the antrum of rats in large numbers and induce no significant inflammatory response. Thus, the direct effect of Helicobacter infection on gastric physiology, independent of gastritis, could be studied. Basal, freely fed and stimulated acid and gastrin levels were recorded from animals infected with H. felis, H. heilmannii or uninfected controls over a 30 week period. No significant difference was found between freely fed gastrin over 7 weeks or fasting gastrin over 24 weeks or basal and stimulated acid over 30 weeks between all three groups. Triple therapy did not alter gastrin or acid output. The antrum of all Helicobacter-infected rats was well colonized; triple therapy cleared H. felis but not H. heilmannii. Very little inflammation was seen in control or Helicobacter-infected animals. In conclusion, Helicobacter-induced effects on gastric physiology are unlikely to be due to direct bacterial effects, but are best explained by other factors (i.e. inflammatory damage).
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PMID:Gastrin release and gastric acid secretion in the rat infected with either Helicobacter felis or Helicobacter heilmannii. 973 79


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