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 rise in serum gastrin and pepsinogen I after 5 days' treatment with the proton pump inhibitor pantoprazole (40 mg/day) was examined in eight duodenal ulcer patients with Helicobacter pylori infection and compared with eight in whom it had been eradicated. Before treatment, the post-prandial serum gastrin concentrations were higher in the H. pylori-positive than -eradicated patients (p less than 0.05). The median rise in pre-prandial serum gastrin concentrations on treatment was similar in the H. pylori-positive (41%) and -eradicated patients (45%). The rise in post-prandial serum gastrin was also similar in the H. pylori-positive (81%) and -eradicated patients (69%), resulting in significantly higher gastrin concentrations during treatment in the former. The median rise in serum pepsinogen I on treatment was greater in the H. pylori-positive (114%) than in the -eradicated patients (8%), resulting in significantly higher concentrations during treatment in the former. These observations indicate that eradication of H. pylori may be a means of moderating the hypergastrinaemia caused by acid-inhibitory therapy. They also indicate that H. pylori-related hypergastrinaemia is not due to an increase of the antral surface pH by the bacterium's urease activity.
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PMID:Helicobacter pylori and hypergastrinaemia during proton pump inhibitor therapy. 153 64

The activities of various types of antiulcer agents against Helicobacter pylori strains were determined by an agar dilution method. Among the compounds tested, benzimidazole proton pump inhibitors were found to have significant activity against this organism. The activity of lansoprazole was fourfold more potent than that of omeprazole and bismuth subsalicylate, with MICs ranging from 1.56 to 25 micrograms/ml. Exposure of Helicobacter pylori to lansoprazole led to an extensive loss of viability as well as suppression of virulence factors such as motility, adhesiveness to epithelial cells and urease activity. The combination of lansoprazole with antimicrobial agents such as penicillins, cephalosporins, macrolides, tetracyclines, aminoglycosides, quinolones, metronidazole and bismuth subsalicylate generally had an additive effect on inhibition of Helicobacter pylori growth.
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PMID:Antibacterial properties of lansoprazole alone and in combination with antimicrobial agents against Helicobacter pylori. 755 27

Helicobacter pylori eradication therapy combining amoxicillin (AMPC), plaunotol (PL), and a proton pump inhibitor (PPI) was examined as an alternative to triple therapy, which has a high rate of side effects and low patient compliance. Thirty-two H. pylori-positive patients (24 men, 8 women) with duodenal ulcers were examined. The diagnosis of H. pylori infection was made by the urease test on specimens biopsied from two sites in the stomach. Simultaneously, the IgG antibody against H. pylori was measured by the EIA method. The therapeutic regimen was lansoprazole (LPZ) 30 mg q.d. (6 weeks) and AMPC 1,500 mg t.i.d. (2 weeks) plus PL320 mg b.i.d. (6 weeks). The rate of ulcer healing was judged endoscopically after 6 weeks. Cases that become urease-negative after the cessation of the therapy were defined as having achieved clearance, and those negative after 1 month as eradication. Within 6 weeks, 31 of 32 patients had healed ulcers. All patients were H. pylori antibody-positive before therapy. The clearance rate was 71.9% (23/32) and the eradication rate was 45.8% (11/24). Adverse effects were observed only in one case. We conclude that combination therapy with LPZ, AMPC, and PL has a high therapeutic effect on ulcer healing and moderate effectiveness for eradication of H. pylori.
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PMID:Eradication of Helicobacter pylori with lansoprazole, amoxicillin, and plaunotol in duodenal ulcer patients. 759 29

We investigated the eradication and recurrence rate of Helicobacter pylori-infected gastric ulcer patients by combination therapies. Eighty-six H. pylori-positive gastric ulcer patients were assigned randomly to one of seven groups: I, omeprazole 20 mg (n = 9); II, lansoprazole (LPZ) 30 mg (n = 16); III, LPZ 30 mg plus plaunotol 480 mg (n = 13); IV, LPZ 30 mg plus ecabet sodium 2 g (n = 11); V, LPZ 30 mg plus clarithromycin 600 mg (the first 2 weeks; n = 11); VI, LPZ 30 mg plus plaunotol 480 mg plus clarithromycin 600 mg (the first 2 weeks; n = 13); and VII, LPZ 30 mg plus ecabet sodium 2 g plus amoxicillin 1,500 mg (the first 2 weeks; n = 13). All therapy was for 8 weeks except where otherwise noted. H. pylori eradication rates as diagnosed by culture, histology, urease test, and [13C]urea breath test 4 weeks after stopping therapy were 0, 0, 8, 45, 6, 46, and 62%, respectively, in groups I-VII. No patient achieving H. pylori eradication suffered recurrence. The combination therapies with proton pump inhibitors in addition to antibiotics and antiulcer agents are safe and effective in H. pylori eradication.
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PMID:Combination therapies with a proton pump inhibitor for Helicobacter pylori-infected gastric ulcer patients. 759 30

The recognition of Helicobacter pylori (H. pylori) as a major cause of gastroduodenal diseases has led to the use of antibiotics to treat these diseases. However, antibiotics used alone are not very effective, and adjuvant therapy is required. The most potent adjuvant therapy consists of increasing the stomach pH with proton pump inhibitors (PPIs). In addition to this action on stomach pH, PPIs, and especially lansoprazole, have been found to have antimicrobial activity against H. pylori. At high concentrations, they are even bactericidal. Furthermore, they can inhibit H. pylori urease activity. These properties, as well as their antisecretory activity, provide the grounds for their use in eradication of H. pylori.
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PMID:Adjuvant therapy for Helicobacter pylori eradication: role of lansoprazole shown in vitro. 767 10

The activities of various types of anti-ulcer agents against Helicobacter pylori (Hp) strains were determined using an agar dilution method. Among the compounds tested, proton pump inhibitors were found to exhibit significant activity against this organism. The activity of lansoprazole was four times more potent than that of omeprazole and bismuth subsalicylate, with MICs ranging from 1.56 to 25 micrograms/ml. Exposure of Hp to lansoprazole led to extensive loss of viability and suppression of virulence factors such as motility, adhesiveness to epithelial cells, and urease activity. Lansoprazole produced aberrant bacterial morphology characterized by elongation and constriction of the cells and collapse of cell surface structures. The combination of lansoprazole with antimicrobial agents such as penicillins, cephalosporins, macrolides, tetracyclines, aminoglycosides, quinolones, and metronidazole produced an additive or synergistic growth inhibition of Hp.
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PMID:Antibacterial properties of lansoprazole alone and in combination with antimicrobial agents against Helicobacter pylori. 767 12

The proton pump inhibitors omeprazole and lansoprazole and its acid-activated derivative AG-2000, which are potent and specific inhibitors of urease of Helicobacter pylori (K. Nagata, H. Satoh, T. Iwahi, T. Shimoyama, and T. Tamura, Antimicrob. Agents Chemother. 37:769-774, 1993), inhibited the growth of H. pylori. The growth was inhibited not only in urease-positive clinical isolates but also in their urease-negative derivatives which had no urease polypeptides. AG-1789, a derivative of lansoprazole with no inhibitory activity against H. pylori urease, also inhibited the growth of both strains even more strongly than the urease inhibitors lansoprazole and AG-2000. Furthermore, the antibacterial activity of omeprazole and lansoprazole was not affected by glutathione or dithiothreitol, which completely abolished the inhibitory activity of lansoprazole against H. pylori urease. These results indicated that the inhibitory action of these compounds against the growth of H. pylori was independent from the inhibitory action against urease.
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PMID:Inhibitory action of lansoprazole and its analogs against Helicobacter pylori: inhibition of growth is not related to inhibition of urease. 772 37

Recently many reports have shown a strong association between Helicobacter pylori infection in the stomach and recurrent peptic ulcer. Moreover, prospective cohort serological studies showed that H. pylori infected individuals have significantly increased rate of gastric cancer in the USA. H. pylori is a gram-negative spiral organism which has urease activity and produces ammonia and CO2 from urea, and nestles in the gastric pits and overlaying mucus gel layer. Many diagnostic methods of H. pylori infection are available; ie bacterial culture, 13C-urea breath test, histology, serum IgG antibody against H. pylori. We developed a new method, ie tissue IgA antibody against H. pylori and detection of H. pylori DNA in the gastric juice by PCR method. Triple therapies with metronidazole, bismuth compounds, and amoxicillin or tetracyclin are difficult to use in Japan because of their sever side effects. Thus, new methods with proton pump inhibitor (PPI) and amoxicillin have been introduced. We treated 14 patients of whom were H. pylori positive-active peptic ulcer with 30 mg/day of lansoprazole, a new PPI, plus 1,500 mg/day of amoxicillin for 2 weeks and 8 (57%) patients were eradicated. Gastric carcinogenesis are multi-steps and multifactorials process. Hypothetical sequence of intestinal type of gastric cancer is that superficial gastritis-->atrophic gastritis-->intestinal metaplasia-->dysplasia-->gastric cancer and H. pylori infection may play a role in the early stage of the sequence. We examined mucosal IgA antibody against H. pylori in chronic gastritis and intestinal metaplasia detected by the Tes-Tape method in 25 resected specimens after gastrectomy for gastric cancer. Positivity rates of tissue H. pylori IgA antibody were lower in the mucosa of intestinal metaplasia than in non-metaplastic gastric mucosa and were negative in carcinoma. Causal relationship between H. pylori infection and gastric cancer is not proven and factors other than H. pylori infection are also important in the gastric carcinogenesis. Finally we introduce 2 reports: (1) NIH Consensus Conference: Helicobacter pylori in peptic ulcer disease (JAMA. 1994; 272: 65-69). The consensus panel concluded that 1. ulcer patients with H. pylori infection require treatment with antimicrobial agents in addition to antisecretory drugs whether on first presentation with the illness or on recurrence; 2. the value of treating nonulcerative dyspepsia patients with H. pylori infection remains to be determined; and 3. the interesting relationship between H. pylori infection and gastric cancer requires further exploration. (2) World Health Organization: Working Group Meeting (Reported in World Congress of Gastroenterology, Los Angeles, 1994). H. pylori plays a causal role in the chain of events leading to cancer of the stomach. Group I: definite carcinogen.
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PMID:[Helicobacter pylori in peptic ulcer and gastric cancer]. 785 88

Since Helicobacter pylori is isolated very frequently from gastric ulcer specimens, the combination therapy of antimicrobial agent and proton pump inhibitor has recently been used. A study was made on whether cefdinir (CFDN), amoxicillin (AMPC), metronidazole (MNZ), omeprazole (OPZ), and omeprazole-M (OPZ-M) have antimicrobial activity against H. pylori and whether they can inhibit H. pylori-producing urease. 1) CFDN, AMPC and MNZ showed a potent antimicrobial activity against H. pylori, and especially, AMPC showed a marked bactericidal activity in a short time. 2) OPZ is reported to be converted to OPZ-M, and active form, in the body. OPZ and OPZ-M showed a moderate antimicrobial activity against H. pylori, and scarcely any bactericidal activity. 3) CFDN and OPZ or AMPC and OPZ in combination did not show any synergistic effect on the antimicrobial activity, but MNZ and OPZ in combination showed additive effect on the antimicrobial activity against H. pylori. 4) OPZ and OPZ-M inhibited H. pylori-producing urease and the inhibitory effect of OPZ-M was more stronger than that of OPZ. CFDN, AMPC and MNZ did not show any inhibitory effect on H. pylori-producing urease at 10 micrograms/ml. From these data, antimicrobial agents and proton pump inhibitors in combination are expected to exert the in vivo synergistic effect since these drugs eradicate H. pylori and inhibit H. pylori-producing urease.
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PMID:[Antibacterial activity of cefdinir and omeprazole against Helicobacter pylori and their inhibition on H. pylori-producing urease]. 840 93

The gastric proton pump inhibitor lansoprazole, its active analog AG-2000, and omeprazole dose dependently inhibited urease activity extracted with distilled water from Helicobacter pylori cells; the 50% inhibitory concentrations were between 3.6 and 9.5 microM, which were more potent than those of urease inhibitors, such as acetohydroxamic acid, hydroxyurea, and thiourea. These compounds also inhibited urease activity in intact cells of H. pylori and Helicobacter mustelae but did not inhibit ureases from other bacteria, such as Proteus vulgaris, Proteus mirabilis, and Providencia rettgeri. The mechanism of urease inhibition was considered to be blockage of the SH groups of H. pylori urease, since SH residues in the enzyme decreased after preincubation with lansoprazole and glutathione or dithiothreitol completely abolished the inhibitory action. The SH-blocking reagents N-ethylmaleimide and idoacetamide were also examined for their inhibition of the urease activity; their 50% inhibitory concentrations were 100- to 1,000-fold higher than those of lansoprazole. These results suggest that lansoprazole and omeprazole can potently and selectively inhibit H. pylori urease and that inhibition may be related to earlier findings indicating that these compounds have selective activity against HP growth.
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PMID:Potent inhibitory action of the gastric proton pump inhibitor lansoprazole against urease activity of Helicobacter pylori: unique action selective for H. pylori cells. 849 73


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