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

We conducted a 12-week, double-blind, randomized, placebo-controlled trial to determine whether cimetidine (300 mg with meals and at bedtime) or a convenient, liquid aluminum-magnesium antacid regimen (15 ml one hour after meals and at bedtime) would expedite healing or relief of symptoms in patients with benign gastric ulcer. Of the 101 patients who completed the trial according to protocol, 32 received the antacid, 36 cimetidine, and 33 placebo. At 4, 8, and 12 weeks after entry, ulcers had healed in a larger percentage of patients treated with cimetidine than of those treated with placebo: 53, 86, and 89 per cent of the cimetidine group versus 26, 58, and 70 per cent of the placebo group (P = 0.02, 0.01, 0.05), respectively. Healing at the three intervals had occurred in 38, 70, and 84 per cent, respectively, of the antacid-treated patients. Neither cimetidine nor antacid was more effective than placebo in relieving symptoms. The presence or absence of symptoms during the fourth and eighth treatment weeks was a poor predictor of the presence of absence of an ulcer crater. We conclude that cimetidine significantly hastens the healing of benign gastric ulcer.
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PMID:Healing of benign gastric ulcer with low-dose antacid or cimetidine. A double-blind, randomized, placebo-controlled trial. 634 44

In view of contradictory reports on the bioavailability of cimetidine in the presence of concomitantly administered antacids we studied the areas under the plasma concentration time curves (AUC) of cimetidine, the maximal concentrations (cmax) and the time, at which cmax was reached (tmax) in eight patients (five patients with duodenal ulcer, three patients with gastric ulcer) with and without the administration of an aluminum hydroxide magnesium hydroxide containing antacid (Maaloxan). No significant effects of the antacid on AUC, cmax and tmax of cimetidine were found. In vitro studies also showed no adsorption of cimetidine to aluminum hydroxide, magnesium hydroxide or the antacid.
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PMID:Absence of in vivo and in vitro interactions of an aluminum hydroxide, magnesium hydroxide containing antacid with cimetidine in patients with peptic ulcer. 661 16

The binding moiety of sucralfate to gastric mucosal sites, such as gastric ulcers and areas of gastritis, was studied in humans. The methods used to elucidate this binding were chemical assay of sucralfate, gastroscopic examination, and histological diagnosis in 39 patients with gastric ulcer and ten patients with gastritis. Sucralfate was observed in the gastric ulcer, and sucrose sulfate ester and aluminum were detected selectively in the lesions. In cases of chronic gastritis, there was no correlation between histological changes and the binding of the sucralfate, but the amount of adhesive mucus and the state of congestion were significantly correlated with the binding of sucralfate.
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PMID:Specific binding of sucralfate in gastric ulcer and gastritis. 668 56

14C-Sucralfate, a basic aluminum salt of 14C-sucrose sulfate, or potassium 14C-sucrose sulfate was administered orally to rats with acetic acid-induced gastric ulcer. The radioactivities representing specific binding of the sucrose sulfate moiety were found significantly higher in ulcer sections of the stomach, with the mean within-animal ulcer/non-ulcer ratio attaining 6, 7, 12 and 2.5, respectively, at 1, 3, 6 and 24 h after 14C-sucralfate administration. Microautoradiography provided direct in vivo evidence for binding of the 14C-sucrose sulfate moiety to exuded proteins resulting in effect in formation of a pepsin-resistant barrier over the surface of an ulcer crater. No comparable findings were obtained in the area of normal mucosa. The administration of 14C-sucralfate was associated with much greater and longer-sustained binding to the ulcer lesion and retention in the stomach and duodenum than simple administration of the soluble potassium salt. These findings not only demonstrate therapeutically significant effects of basic aluminum compoundation but also substantiate likely differences from pepsin inhibitors such as amylopectin sulfate in terms of presence or absence of adhesiveness, local barrier effects, and long duration of actions.
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PMID:Selective binding of sucralfate to ulcer lesion. II. Experiments in rats with gastric ulcer receiving 14C-sucralfate or potassium 14C-sucrose sulfate. 689 77

To determine whether the previously reported mechanisms of action of sucralfate for gastric ulcer are also operative in duodenal ulcer, a single dose of 14C-labelled sucralfate was administered orally to rats with acetic acid-induced duodenal ulcer. Adhesive coating with sucralfate was visible over the duodenal lesion for 6 h in the majority of animals and found localized increasingly selective to the ulcerous area following administration. Visual observations were supported quantitatively by greater than unity mean within-animal ulcer/non-ulcer ratios of binding by 14C-sucrose fulfate moiety and aluminum, with statistical significance at 3 and 6 h post-administration (P less than 0.01 or 0.05). While the aluminum component was found persistent relative to the sucrose sulfate moiety in the adhesive coating, an additional in vitro study revealed that this was due to the pH of duodenal contents and did not lead to a loss of adhesiveness. In addition to these results, the buffering potential of sucralfate coating to control the local pH condition sufficient for binding to ulcer surface proteins to occur support the conclusion that the same mechanisms of action of sucralfate commonly apply to gastric and duodenal ulcers.
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PMID:Selective binding of sucralfate to ulcer lesion. III. Experiments in rats with duodenal ulcer receiving 14C-sucralfate. 689 78

Sucralfate is a basic aluminum salt of a sulfated disaccharide. In this study, patients with gastric ulcer were given oral multiple doses of sucralfate prior to partial gastrectomy, and binding of the drug to the ulcer lesion and to nonulcerated mucosa was estimated by chemical determination of aluminum and sulfated disaccharide. The ulcerated mucosa was found to contain, on the average, 6-7 times more sucralfate per square centimeter than the control mucosa (P less than 0.01 and less than 0.05 for aluminum and sulfated disaccharide, respectively). The high affinity of sucralfate for ulcerated mucosa, particularly the sucrose sulfate moiety, supports previous data that the beneficial effect of sucralfate in ulcer disease is due in part to complex formation between sucrose sulfate and proteins at the ulcer site.
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PMID:Selective binding of sucralfate to gastric ulcer in man. 689 71

A randomized controlled clinical study was conducted to determine (a) whether basic aluminum sucrose sulfate (sucralfate) is effective in preventing or reducing gastric ulcer recurrence, and (b) the clinical parameters contributing to ulcer recurrence after endoscopically proved healing has been effected. A total of 167 patients were assigned on a random basis to either of two treatment groups, control (aluminum hydroxide and magnesium oxide) or sucralfate, and given these medications for 6 months. At the end of this period all medication was withdrawn from both groups and the patients were followed for an additional 12 months. Each patient was examined endoscopically at bimonthly intervals throughout the 18-month observation period. Treatment (sucralfate), ulcer history, size of previous ulcer(s), prestudy healing time, and prestudy healing stage attained (red or white scarring) were associated with a significant reduction in recurrence rate. Ulcer recurrence was markedly reduced in sucralfate patients as compared to control when the pretreatment ulcers had healed slowly (P less than 0.001).
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PMID:Endoscopic evaluation of the effect of sucralfate therapy and other clinical parameters on the recurrence rate of gastric ulcers. 698 40

Gastric ulcer induced by the injection of acetic acid (0.025 ml of 20%) into the gastric wall of rats was healed considerably 5 days after the injection of acetic acid. Non-steroidal anti-inflammatory drugs (NSAID) such as aspirin, indomethacin, and phenylbutazone were given consecutively for 5 days, and they exacerbated the ulcer and enlarged the ulcer area. Aspirin caused exacerbation when it was given for the initial 5 days of the ulcer healing process. Phenylbutazone caused exacerbation by the administration for 5 days at the middle stage of the ulcer healing process. In contrast, indomethacin caused exacerbation not only when it was given for the initial 5 days but also when it was given for the middle 5 days. The effect of the antiulcer agent N-acetyl-L-glutamine aluminum complex (KW-110) on the exacerbation was studied. KW-110 at an oral dose of 500 mg/kg inhibited remarkably the exacerbation induced by all of the NSAID used. The development of gastric lesions induced by these NSAID was also prevented by KW-110. Further study was carried out with regard to the influences of KW-110 on the pharmacological properties of NSAID. The results showed no influences of KW-110 on the antiedematous and antipyretic actions of the NSAID.
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PMID:Effect of N-acetyl-L-glutamine aluminum complex (KW-110), an antiulcer agent, on the non-steroidal anti-inflammatory drug-induced exacerbation of gastric ulcer in rats. 709 47

Sodium polyacrylate (PANa) is a water-soluble, high-molecular compound, and its aqueous solution shows a very high viscosity and stringiness. In the present study, preventive effects of PANa on three kinds of esophageal lesions induced by gastric juice were examined in comparison with those of aceglutamide aluminum and sodium alginate. The influences of PANa on gastric contents were also studied. The preventive effect of PANa given intraesophageally on esophageal lesions induced by the intraesophageal application of gastric juice was more potent than aceglutamide aluminum and sodium alginate. Oral administration of PANa inhibited the formation of esophageal ulcer by pylorus ligation more markedly than aceglutamide aluminum, whereas sodium alginate had no effect in a high dose of 500 mg/kg. In preventing gastric ulcer which occurred simultaneously with the esophageal ulcer after the pylorus ligation, aceglutamide aluminum was most potent, and PANa was as potent as sodium alginate. Oral administration of PANa showed a more protective effect than aceglutamide aluminum on the esophageal ulceration induced by the simultaneous ligations of the pylorus and limiting ridge, whereas sodium alginate in a high dose of 500 mg/kg had little effect on the ulcer formation. PANa caused only a slight increase in the pH of gastric juice and a slight decrease in pepsin activity. From the results, it may be concluded that PANa showed an antiulcerogenic activity mainly due to its mucosa covering action against gastric juice.
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PMID:Effects of sodium polyacrylate (PANa) on acute esophagitis by gastric juice in rats. 710 49


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