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)

The efficacy of antacid in the treatment of benign gastric ulcer is less well established than in the treatment of duodenal ulcer. The objective of this study was to monitor ulcer healing and symptom relief in 38 patients with gastric ulceration treated for 6 weeks with cimetidine (Tagamet) 300 mg q.i.d. or an aluminum-magnesium containing antacid (Mylanta II) 10 ml q.i.d. (acid neutralizing capacity 203.2 mEq/day). The study was single-blind; the study physicians and those providing endoscopic assessments were not aware of the patients' treatment. Entered into the study were 19 male and 19 female patients ranging in age from 17 to 70 years, with a mean age of 52 years. None of the patients had taken cimetidine in the previous month, and none abused alcohol or nonsteroidal anti-inflammatory agents, but two-thirds of the patients were smokers. Five patients in the antacid group withdrew for numerous reasons including continued pain, noncompliance, and side effects. All patients in the cimetidine group completed the study, and no side effects were noted. There was no difference between the antacid- and the cimetidine-treated patients in the relief of symptoms. There was a significant difference in the 6-week ulcer healing between the groups, with 14/19 (74%) healed in the cimetidine group compared with only 6/14 (43%) healed in the antacid group (p less than 0.025). Thus, Mylanta II, 10 ml four times daily, is comparable to cimetidine 300 mg q.i.d. in the symptomatic relief of benign gastric ulceration, but ulcer healing was superior using cimetidine.
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PMID:Comparative study of cimetidine and Mylanta II in the 6-week treatment of gastric ulcer. 389 94

In this retrospective study, a cohort of gastric ulcer patients treated with antacids was compared with a well-matched group of patients treated with a combination of antacids and cimetidine. Cimetidine combined with antacids enhanced gastric ulcer healing, thereby significantly reducing the number of gastric ulcer operations. Cimetidine appears to act by providing a less acidic environment in which gastric ulcers can heal. The exact mechanism of cimetidine's action on gastric ulcers is not clear. Nonprophylactic administration of cimetidine apparently has no effect on the recurrence rate of gastric ulcers.
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PMID:Effect of cimetidine on healing and surgical treatment of gastric ulcers. 399 50

Although increased gastric acidity may be important in the pathogenesis of duodenal ulcer, it has a less well-defined role in the formation of gastric ulcers. The present study was undertaken to determine (1) the 24-hour intragastric pH and serum gastrin profiles of 31 patients with duodenal ulcers, eight patients with gastric ulcers, and seven healthy volunteers and (2) the effect of 600 mg of cimetidine BID on these measurements. There was considerable overlap of basal acid output values in the three groups, and mean values did not differ significantly. In response to pentagastrin, the peak acid output was significantly higher in the duodenal ulcer group than in the gastric ulcer or healthy group. There were no intergroup differences in intragastric hydrogen ion (H+) activity after meals, overnight, and over 24 hours, when all subjects received placebo. However, the pH values remained at or above 4.0 for a longer period during the night in the gastric ulcer patients than in the duodenal ulcer patients or healthy subjects. There were no intergroup differences in basal gastrin concentration, but the postprandial gastrin response after each meal was higher in the gastric ulcer group than in the other two groups. In the gastric ulcer group, cimetidine suppressed H+ activity at all times; in the duodenal ulcer and healthy groups, cimetidine suppressed H+ activity only after breakfast, overnight, and over 24 hours. Cimetidine enhanced the serum gastrin response to food to a greater extent in the ulcer patients than in the healthy subjects. In the healthy subjects, the ratio of H+ to gastrin (H+:G) was higher than in the duodenal or gastric ulcer patients but was suppressed only minimally by cimetidine, whereas cimetidine markedly suppressed the H+:G ratio in both groups of ulcer patients. Patients with a history of duodenal or gastric ulcers differed from healthy volunteers in their food-stimulated gastrin response and in their H+:G ratio when treated with cimetidine. Intergroup differences in gastrin response to food, but not in intragastric pH in response to food, suggests that defective control of or response to gastrin may be important in the pathogenesis of acid-peptic disease. Cimetidine, which was effective in H+ suppression in all subject groups, may alter the sensitivity of the parietal cells to gastrin in patients with duodenal or gastric ulcers.
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PMID:Interrelationship between gastric acidity and gastrin concentration in patients with duodenal or gastric ulcer and in healthy subjects. 401 26

The fasting concentrations of total gastrin and gastrin-17 (G-17) were similar in healthy volunteers and in asymptomatic patients with gastric ulcers or duodenal ulcers. However, the fasting serum concentration of gastrin-34 (G-34) was higher in patients with gastric ulcers than in normal subjects, in whom it was higher than in patients with duodenal ulcers. In response to food, the increases in G-17, G-34, and total gastrin were greater in ulcer patients than in healthy subjects. Cimetidine administration was associated with further increases in G-17, G-34, and total gastrin in normal subjects and gastric ulcer patients after meals. The ratio G-17/G-34 was similar in placebo-treated normal subjects and placebo-treated patients with gastric or duodenal ulcers. Cimetidine produced an increase in G-17/G-34 in placebo-treated normal subjects and placebo-treated patients with gastric or duodenal ulcers, but the ratio G-17/G-34 was greater in patients with gastric ulcers than in normal subjects. These results indicate that: differences in serum gastrin concentrations between patient groups, treatment regimens, and time of day are better detected by measuring G-17 and G-34 rather than total gastrin; there are differences in fasting and food-stimulated gastrin concentrations between normal subjects and patients with gastric or duodenal ulcers; the fasting concentration of G-34 is higher than G-17 in normal subjects and patients with gastric ulcers but not in patients with duodenal ulcers; food increases G-17 in all subjects but G-34 only in subjects with gastric ulcers; cimetidine increases the fasting concentration of total gastrin in normal subjects and patients with gastric ulcers and increases G-17 and G-34 in normal subjects; cimetidine increases the ratio G-17/G-34 in normal subjects and patients with gastric ulcers, but decreases G-17/G-34 in patients with duodenal ulcers. It is proposed: that measurements of total gastrin concentration should be replaced by measurements of G-17 and G-34 and that such measurements of G-17 and G-34 indicate differences in serum gastrin concentrations between normal subjects and those with peptic ulcers and between those with gastric versus duodenal ulcers. The role of altered gastrin metabolism in the pathogenesis of ulcers needs to be established.
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PMID:Postprandial changes in serum concentrations of gastrin-17, gastrin-34, and total gastrin in patients with duodenal or gastric ulcers and in normal subjects. 407 62

The development of the histamine-H2-receptor-antagonist cimetidine has led to a better understanding in the physiological control of gastric secretion and to a new approach in the management of various lesions of the upper gastrointestinal tract. Numerous world-wide controlled clinical trials have shown that the new drug is more efficient in diseases which are accompanied by hyperchlorhydria. This is especially true in the acute therapy and long-term prophylaxis of duodenal ulcer and in Zollinger-Ellison-syndrome. In contrast, at the present, the therapeutic benefit of cimetidine is less proven in gastric ulcer, in reflux oesophagitis and in acute hemorrhage of the upper gastrointestinal tract. Even under long-term administration no severe organic side effect occured with the drug which generally is well tolerated. Cimetidine appears as a valuable and safe agent, when the range of application is limited to defined gastrointestinal disorders.
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PMID:[Review: cimetidine: mode of action and clinical efficacy in various gastrointestinal diseases (author's transl)]. 610 88

The effects of somatostatin on ulcer formation, gastric acid secretion and histamine release were assessed during vagus nerve stimulation in rats. Direct electrical vagal stimulation significantly increased histamine release and acid output in gastric secretion but decreased mast cell counts in gastric glandular mucosa. Hemorrhagic ulceration on the gastric glandular mucosa was also observed. Somatostatin pretreatment (10 micrograms/kg) did not inhibit gastric ulcer formation, gastric acid secretion or histamine release induced by vagal stimulation. Cimetidine (an H2 blocker) pretreatment, however, significantly decreased gastric acid secretion as well as ulcer formation. The present study indicates the direct vagal stimulation increases gastric acid secretion and ulcer formation. These effects are partially histamine dependent. Somatostatin did not inhibit histamine release induced by vagal stimulation and reflects the inability of the drug to prevent ulcer formation and gastric output under these conditions in rats. However, the inhibition of basal gastric acid secretion produced by somatostatin might be useful clinically in humans.
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PMID:The lack of effects of somatostatin on gastric responses induced by electrical vagal stimulation. 614 Jun 85

In view of the findings that Cimetidine, used in the treatment of gastric ulcers, blocks histamine-type 2 receptors, which are also present on T suppressor lymphocytes, a study was carried out in a 65-year-old male suffering from giant benign gastric ulcer and in parallel for control purposes in a healthy male of the same age. T suppressor cells obtained from peripheral blood of the patient were tested prior to institution of treatment with Cimetidine and 21, 62 and 100 days thereafter using 3 different tests - theophylline sensitivity, monoclonal antibodies OKT4 and OKT8 and as a functional test a local xenogeneic graft-versus-host reaction (GVHR). The number and percentage of T suppressor cells, which were high before treatment, showed a significant decrease after two months of treatment and this was paralleled by a decrease in suppressor activity and reversal of the functional activity of the T cells from negative to normal. Helper cells were normal before and after treatment. At the same time the patient showed a marked clinical improvement, with healing of the ulcer evidenced by endoscopy. It is suggested that Cimetidine may effect healing by influencing immune mechanisms.
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PMID:Effect of cimetidine on T lymphocytes in a patient with giant benign gastric ulcer. 624 Nov 62

In August 1977 a patient developed herpes zoster just before she commenced a course of cimetidine (Tagamet; Smith, Kline & French) for a chronic gastric ulcer. She experienced both rapid relief of the ulcer symptoms and, rather unexpectedly, dramatic relief of the herpetic pain and rapid disappearance of the eruption. On the basis of this observation cimetidine was prescribed to 21 patients with herpes zoster. The results continued to be encouraging in all but 3 patients. The trial was therefore extended to other herpesvirus infections. In all but 1 of 7 patients with herpes labialis the blisters were aborted, and in 1 patient with herpes keratitis the result was also encouraging, the attacks being markedly shortened in duration and reduced in frequency. The results of this preliminary trial warrant a systematic scientific inquiry into the potential role of cimetidine in the treatment of hypesvirus infection, as well as a study of the mechanisms involved.
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PMID:Cimetidine in the treatment of herpesvirus infections. 625 Feb 37

Today, we have effective and potent drugs such as H2-receptor antagonists for the treatment of peptic ulcers. Cimetidine and ranitidine are antisecretory drugs which heal 67-90% of duodenal ulcers in 4 weeks. Certain prostaglandins (PGs) which also heal gastroduodenal ulcers and hemorrhagic gastritis not only diminish gastric acid secretion but also confer unique protective properties on the gastroduodenal mucosa. This phenomenon of 'cytoprotection' is supported by the experimental finding that PGs prevent gastroduodenal mucosal injury caused by absolute ethanol, HCl, NaOH and other irritating agents. Other PGs which do not reduce gastric acid secretion also heal human gastroduodenal ulcers. These special properties of PGs make them potentially beneficial for the treatment of gastric ulcer, and gastroduodenal ulcers accompanying use of nonsteroidal anti-inflammatory drugs as well as hemorrhagic gastritis which is particularly refractory to other therapeutic modalities.
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PMID:Prostaglandins, gastroduodenal ulcer and hemorrhagic gastritis. 633 8

Most reports of interactions involving analgesics deal with their effects on the actions of other drugs rather than vice versa. Aspirin and ethanol have synergistic effects on the development of gastritis, gastrointestinal bleeding, and chronic gastric ulcer. This must be the most common and most important interaction affecting analgesic toxicity. Combined overdosage of aspirin with central nervous system depressants may be particularly hazardous because suppression of the salicylate-induced respiratory stimulation further shifts the disordered acid-base balance towards acidosis. The toxicity of acetaminophen (paracetamol) depends primarily on the balance between the rate of formation of the hepatotoxic metabolite and the rate of glutathione synthesis in the liver. In animals, prolonged pretreatment with ethanol increases the metabolic activation and acute toxicity of acetaminophen, and there is some evidence that chronic alcoholics are more susceptible to hepatotoxicity following acute overdosage. It has been assumed that this sensitivity in chronic alcoholics is due to microsomal enzyme induction with enhanced metabolic activation of acetaminophen. However, the metabolic activation of acetaminophen, as judged by the urinary excretion of its cysteine and mercapturic acid conjugates, is not increased in heavy drinkers or in patients induced by long-term treatment with anticonvulsants or rifampicin. Microsomal enzyme induction is complex. There are important species differences and different agents may selectively induce different variants of the multiple forms of cytochrome P-450. The acute administration of ethanol greatly reduces the metabolic activation of acetaminophen in heavy drinkers with more than a 50 percent decrease in cysteine and mercapturic acid conjugate production. Thus ingestion of ethanol should reduce the risk of liver damage following acetaminophen overdosage. Cimetidine, which inhibits the oxidative metabolism of some drugs, reduces the hepatotoxicity and increases the dose of acetaminophen in mice required to kill 50 percent of the animals. However, contrary to expectations, cimetidine does not inhibit the oxidative metabolism of acetaminophen in man. Salicylamide competes with acetaminophen for sulphate conjugation but is unlikely to potentiate toxicity following overdosage since sulphate conjugation is rapidly saturated anyway. Animal studies suggest that the hepatotoxicity of acetaminophen after overdosage may be increased by other agents which deplete glutathione, but there is no information on this point in man.
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PMID:Drug interactions affecting analgesic toxicity. 635 60


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