Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rabeprazole, a new proton pump inhibitor, was studied in patients with acid-peptic-related diseases (duodenal ulcer, gastric ulcer, GERD) in three placebo-controlled, double-blind, randomized clinical trials. Men and women over the age of 18 were enrolled if the presence of an active duodenal or gastric ulcer or erosive or ulcerative esophagitis was confirmed on upper gastrointestinal endoscopy. Patients were randomly allocated to either placebo or rabeprazole 20 mg or 40 mg in the duodenal and gastric ulcer protocols or to placebo or rabeprazole 10 mg, 20 mg, or 40 mg in the GERD protocol. All doses of rabeprazole in all three studies were statistically significantly superior to placebo in healing acid-related lesions. There were no treatment differences between the rabeprazole doses in healing active peptic lesions. The incidence of positive [13C]urea breath test for H. pylori was 53% in patients with duodenal or gastric ulcers. H. pylori status was not effected by treatment with rabeprazole.
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PMID:Rabeprazole in treatment of acid peptic diseases: results of three placebo-controlled dose-response clinical trials in duodenal ulcer, gastric ulcer, and gastroesophageal reflux disease (GERD). The Rabeprazole Study Group. 959 Apr 13

The reverse transcription polymerase chain reaction (RT-PCR) was performed to detect genes of RNA viruses in the freshly biopsied gastric mucosa of seven patients with low gastric acidity. Although nucleoprotein genes of Sendai virus and hemmaglutinin genes of influenza virus A were not detected, nucleoprotein genes of influenza virus B were detected in samples from three of the seven patients. The first patient had had antrectomy and vagotomy for gastric ulcer, the second patient was receiving a histamine type 2 receptor blocker for gastritis, and the third patient was receiving a proton pump inhibitor for gastric ulcer. Virus isolation from gastric mucosa and from gargles was negative for all seven patients. These findings suggest that genes of influenza viruses may exist in the gastric mucosa of patients with low gastric acidity.
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PMID:Detection of genes of RNA viruses from freshly biopsied gastric mucosa by reverse transcription polymerase chain reaction. 960 41

1. Polyriboinosinic-polyribocytidylic acid (Poly I:Poly C), an interferon inducer was studied for its effect on gastric ulceration in rats. Polyriboinosinic-polyribocytidylic acid (1, 2 and 4 mg/kg, i.m.) showed a dose-dependent inhibition of gastric ulcers induced by aspirin, cold restraint stress and pylorus ligation (Shay's model). Protective dose (PD50) +/- SEM values of Poly I:Poly C on these models of ulcers were 1.9 +/- 0.2, 2.3 +/- 0.4 and 2.8 +/- 0.4 (mg/kg, i.m.) respectively. 2. Polyriboinosinic-polyribocytidylic acid (10-60 micrograms) produced dose-dependent inhibition of gastric proton pump (H+/K(+)-ATPase) activity in the gastric parietal microsomal fraction. The concentration of Poly I:Poly C causing a 50% inhibition (IC50) +/- SEM was found to be 17.6 +/- 1.2 micrograms. 3. Polyriboinosinic-polyribocytidylic acid caused a significant decrease in free and total acid and pepsin and an increase in mucin content in Shay (pylorus-ligated) rat. 4. Polyriboinosinic-polyribocytidylic acid did not exert a significant influence on isolated tissue preparations for anti-cholinergic (acetylcholine-induced contraction of guinea-pig ileum) and H2-anti-histaminic (histamine-induced contraction of rat uterus and guinea-pig auricle) activities. 5. Thus, the present study indicates that Poly I:Poly C may possess anti-gastric ulcer activity as a result of inhibition of the gastric proton pump.
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PMID:Interferon-inducer polyriboinosinic-polyribocytidylic acid: a potent anti-gastric ulcer agent and inhibitor of the gastric proton pump in rats. 967 29

Lansoprazole is the new proton pump inhibitor, decreasing the volume of gastric acid secretions and inhibiting secretion of gastric acid and pepsin. Lansoprazole appears to be more effective in therapy of gastric ulcer and duodenal ulcer in comparison with H2-receptor antagonists and omeprasole. Reflux oesophagitis and Zollinger-Ellison syndrome are also healed by Lansoprazole. The best results in the treatment of patients with peptic ulcer, reflux oesophagitis and Zollinger-Ellison syndrome were occurred after a daily 30 mg dose of Lansoprazole. Treatment of patients with duodenal ulcer should be continued for 2 to 4 week and the case of gastric ulcer a well as reflux oesophagitis should be prolonged till 4 to 8 week. Lansoprazole is well tolerated, reported adverse effects are similar to the incidence observed in patients treated with other proton pump inhibitors.
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PMID:[Lansoprazol ++ : a new proton pump inhibitor]. 977 Oct 21

Proton pump inhibitors (PPIs) are drugs which irreversibly inhibit proton pump (H+/K+ ATPase) function and are the most potent gastric acid-suppressing agents in clinical use. There is now a substantial body of evidence showing improved efficacy of PPIs over the histamine H2 receptor antagonists and other drugs in acid-related disorders. Omeprazole 20 mg/day, lansoprazole 30 mg/day, pantoprazole 40 mg/day or rabeprazole 20 mg/day for 2 to 4 weeks are more effective than standard doses of H2-receptor antagonists in healing duodenal and gastric ulcers. Patients with gastric ulcers should receive standard doses of PPIs as for duodenal ulcers but for a longer time period (4 to 8 weeks). There is no conclusive evidence to support the use of a particular PPI over another for either duodenal or gastric ulcer healing. For Helicobacter pylori-positive duodenal ulceration, a combination of a PPI and 2 antibacterials will eradicate H. pylori in over 90% of cases and significantly reduce ulcer recurrence. Patients with H. pylori-positive gastric ulcers should be managed similarly. PPIs also have efficacy advantages over ranitidine and misoprostol and are better tolerated than misoprostol in patients taking nonsteroidal anti-inflammatory drugs (NSAIDs). In endoscopically proven gastro-oesophageal reflux disease, standard daily doses of the PPIs are more effective than H2-receptor antagonists for healing, and patients should receive a 4 to 8 week course of treatment. For severe reflux, with ulceration and/or stricture formation, a higher dose regimen (omeprazole 40 mg, lansoprazole 60 mg, pantoprazole 80 mg or rabeprazole 40 mg daily) appears to yield better healing rates. There is little evidence that PPIs lead to resolution of Barrett's oesophagus or a reduction of subsequent adenocarcinoma development, but PPIs are indicated in healing of any associated ulceration. In Zollinger-Ellison syndrome, PPIs have become the treatment of choice for the management of gastric acid hypersecretion.
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PMID:Proton pump inhibitors. Pharmacology and rationale for use in gastrointestinal disorders. 977 9

The effects of trimebutine maleate (TM), a prokinetic drug, on gastrointestinal motility in patients with gastric ulcer were investigated. Twenty patients with active gastric ulcers were allocated to two groups; 10 patients received a proton pump inhibitor alone (PPI group), given orally, and 10 patients received oral TM in combination with a PPI (PPI + TM group), each for a period of 8 weeks. Electrogastrography (EGG) and gastric emptying were measured before and after the treatment period. During the active ulcer stage, tachygastria (more than 0.06 Hz) or bradygastria (less than 0.04 Hz) in the EGG frequency were observed in 9 patients either before or after meals. During the healed ulcer stage, tachygastria or bradygastria was observed in 4 of 10 patients in the PPI group, while in the PPI + TM group, 1 patient had tachygastria and none had bradygastria. Postprandial dip (PD) was observed in 3 of the 20 patients during the active stage, while after treatment, PD was observed in 3 patients in the PPI group and in 6 patients in the PPI + TM group, respectively. Gastric emptying in the PPI group did not show any change between before and after treatment, while that in the PPI + TM group improved significantly after treatment. These results suggest that TM may have an ameliorative effect on abnormal gastric motility in patients with gastric ulcer.
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PMID:Effects of trimebutine maleate on gastric motility in patients with gastric ulcer. 985 73

Proton pump inhibitor (PPI)-based triple therapy, which combines a PPI and two antibiotics, is highly effective in eradicating Helicobacter pylori infection in peptic ulcer patients, even if given for only 1 week. However, the application of this regimen in patients with bleeding ulcers has not been adequately investigated. We studied the effectiveness of triple therapy in treating 122 patients with proven H. pylori infection, and bleeding stigmata on endoscopy; 97 had duodenal ulcer (DU), 15 had gastric ulcer (GU), and 10 had both types of ulcers. A regimen of omeprazole (20 mg), metronidazole (500 mg), and clarithromycin (250 mg) twice daily was administered for 1 week as soon as the patient could eat normally after bleeding, followed by omeprazole (20 mg) daily for 3 additional weeks. Follow-up endoscopy and 13C-urea breath tests (UBTs) were performed at least 4 weeks after triple therapy. A total of 104 patients completed the study, 83 with DU, 12 with GU, and nine with both. The overall ulcer healing rate was 97.1% and the eradication rate was 91.3%. Patients with and without H. pylori eradication did not differ significantly in terms of age, gender, UBT titer, units of blood transfused, or interval between endoscopy and the beginning of triple therapy. We conclude that 1-week low-dose PPI-based triple therapy is effective in eradicating H. pylori infection in patients with bleeding peptic ulcers. When followed by 3 weeks of additional PPI treatment, a satisfactory ulcer healing rate can also be achieved.
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PMID:One-week low-dose triple therapy is effective in treating Helicobacter pylori-infected patients with bleeding peptic ulcers. 987 28

The treatment of a peptic ulcer occurring in a patient who is taking non-steroidal anti-inflammatory drugs depends on whether or not the patient can readily stop taking the non-steroidal anti-inflammatory drug. If they can, healing is generally rapid, and can be achieved with any effective ulcer-healing agent. When the non-steroidal anti-inflammatory drug cannot be easily stopped, ulcer healing is slower and the treatment of choice is to heal the ulcer with a proton pump inhibitor. The risk of ulceration in patients taking non-steroidal anti-inflammatory drugs can be reduced by two main strategies: the choice of non-steroidal anti-inflammatory drug and its dosage on the one hand, and the use of prophylactic co-therapy on the other. The two are not of course mutually exclusive. It is now clear that not all non-steroidal anti-inflammatory drugs are equally damaging. Several studies have shown that the shorter half life drugs (at least in their recommended dosages) are generally less ulcerogenic. There is clear dose-dependence, so the drugs should be used at the lowest effective dose, and non-steroidal anti-inflammatory drugs should not be given in combination without careful weighing of risks and benefits. Giving either omeprazole or misoprostol concurrently with a non-steroidal anti-inflammatory drug substantially reduces the risk of ulceration. Full dosage histamine H2-receptor antagonists give good protection against non-steroidal anti-inflammatory drug-associated duodenal ulcers, but two large trials with ranitidine showed no protection against gastric ulcer. One study of double dosage famotidine did show a reduction in gastric ulcer incidence as well. Recently, two large randomized trials have compared omeprazole 20 mg daily head-to-head with ranitidine and misoprostol. Overall, the proton pump inhibitor was more effective than the other two for ulcer prevention, although it is interesting that erosions seemed to be prevented better by the prostaglandin. The biggest challenge for clinical judgement is when to use prophylactic co-therapy. Patients for whom this should be especially considered are those who have had a prior ulcer, the elderly, those needing higher non-steroidal anti-inflammatory drug dosage or co-therapy with vascular-protective aspirin, and those whose other medical conditions make them less likely to survive a gastrointestinal haemorrhage or perforation.
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PMID:A clinical approach to management of patients with non-steroidal anti-inflammatory gastropathy. 1037 75

c-Kit is a receptor tyrosine kinase, and it is encoded by the mouse W locus. Mutant W/Wv mice develop spontaneous gastric antral ulcers. The aim of the present study was to investigate the pathogenesis of these gastric ulcers and to examine the effects of two antiulcer drugs; a proton pump inhibitor (2{[4-(3-methoxypropoxy)-3-methylpyridine-2-yl]methyl-sulfinyl}-1H -benzimidazole sodium salt, rabeprazole) and a mucosal protective drug (geranylgeranylacetone, GGA), on the gastric ulcers. The inhibition of the gastric acid secretion by rabeprazole (30 mg/kg body weight, subcutaneous injection once a day for six weeks) significantly increased the gastric ulcer formation compared to the controls. In contrast, the GGA treatment (100 mg/kg body weight, oral administration for six weeks) significantly inhibited the ulcer formation. Bile reflux was seen in these mutant mice, and they showed no cyclic intense contractions in the gastric antrum. These results suggest that bile reflux due to the disturbance of gastric antral movement is a cause of the spontaneous gastric ulcers in W/Wv mice.
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PMID:Bile reflux due to disturbed gastric movement is a cause of spontaneous gastric ulcer in W/Wv mice. 1038 93

Antacids are commonly used self-prescribed medications. They consist of calcium carbonate and magnesium and aluminum salts in various compounds or combinations. The effect of antacids on the stomach is due to partial neutralisation of gastric hydrochloric acid and inhibition of the proteolytic enzyme, pepsin. Each cation salt has its own pharmacological characteristics that are important for determination of which product can be used for certain indications. Antacids have been used for duodenal and gastric ulcers, stress gastritis, gastro-oesophageal reflux disease, pancreatic insufficiency, non-ulcer dyspepsia, bile acid mediated diarrhoea, biliary reflux, constipation, osteoporosis, urinary alkalinisation and chronic renal failure as a dietary phosphate binder. The development of histamine H2-receptor antagonists and proton pump inhibitors has significantly reduced usage for duodenal and gastric ulcers and gastro-oesophageal reflux disease. However, antacids can still be useful for stress gastritis and non-ulcer dyspepsia. The recent release of proprietary H2 antagonists has likely further reduced antacid use for non-ulcer dyspepsia. Other indications are still valid but represent minor uses. Antacid drug interactions are well noted, but can be avoided by rescheduling medication administration times. This can be inconvenient and discourage compliance with other medications. All antacids can produce drug interactions by changing gastric pH, thus altering drug dissolution of dosage forms, reduction of gastric acid hydrolysis of drugs, or alter drug elimination by changing urinary pH. Most antacids, except sodium bicarbonate, may decrease drug absorption by adsorption or chelation of other drugs. Most adverse effects from antacids are minor with periodic use of small amounts. However, when large doses are taken for long periods of time, significant adverse effects may occur especially patients with underlying diseases such as chronic renal failure. These adverse effects can be reduced by monitoring of electrolyte status and avoiding aluminum-containing antacids to bind dietary phosphate in chronic renal failure. Antacids, although effective for discussed indications of duodenal and gastric ulcer and gastro-oesophageal reflux disease, have been replaced by newer, more effective agents that are more palatable to patients. Antacids are likely to continue to be used for non-ulcer dyspepsia, minor episodes of heartburn (gastro-oesophageal reflux disease) and other clear indications. Although their wide-spread use may decline, these drugs will still be used, and clinicians should be aware of their potential drug interactions and adverse effects.
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PMID:Antacids revisited: a review of their clinical pharmacology and recommended therapeutic use. 1040 Apr 1


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