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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of carbenoxolone on the healing of gastric ulcer and erosions was compared with that of placebo. The series consisted of 20 patients with chronic gastric ulcers and 20 patients with superficial erosions of the stomach. The diagnosis as well as the follow-up of the lesions were based on gastroscopic examinations. The ulcers were measured gastroscopically. A double-blind method was used. Besides carbenoxolone 50 mg or placebo three times daily, all the patients received antacids in fixed dosage for six weeks. Subjective symptoms and cardiovascular side-effects were recorded. Maximal acid output and serum gastrin levels were measured before and after the treatment. No difference was seen between carbenoxolone and placebo groups with regard to the healing rate of the ulcers of disappearance of the erosions. The subjective symptoms subsided significantly faster in the treatment groups than in the control groups. No cardiovascular side-effects were evident during the treatment with carbenoxolone. One patient needed potassium supplements. Carbenoxolone had no effect on the pentagastrin-stimulated gastric acid secretion nor on the serum gastrin values.
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PMID:Double-blind study of carbenoxolone in gastric ulcer and erosions. 35 71

Fifty-four outpatients with endoscopically diagnosed benign gastric ulcer were allocated at random to treatment with either cimetidine 800 mg daily for six weeks or carbenoxolone sodium 300 mg daily for one week then 150 mg daily for five weeks. Ulcers were reassessed by endoscopy at the end of the trial. The endoscopist was unaware of the treatment and did not take part in the clinical care of the patients. Twenty-one of the 27 patients (78%) given cimetidine and 14 of the 27 (52%) given carbenoxolone had healed ulcers. Symptomatic response occurred earlier with cimetidine but was not significantly better. Unwanted effects were more common in the carbenoxolone group: 12 patients developed hypokalaemia, four of whom needed oral potassium supplements. The results suggest that histamine H2-receptor blockade is at least as effective as carbenoxolone sodium for benign gastric ulcer and produces fewer side effects.
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PMID:Controlled comparison of cimetidine and carbenoxolone sodium in gastric ulcer. 37 54

Most physicians recognize that the ingestion of lye is associated with severe esophageal damage. It is much less widely known that gastric injury is the predominant finding when acid is ingested. We are reporting on five patients who had severe gastric damage after ingestion of diluted sulfuric acid (three cases), capsules of potassium hydroxide, and Clinitest tablets (one case each). Fiberoptic endoscopy was used to localize the extent and severity of injury and to follow the evolution of the damage. The extent and location of injury varied with the amount and type of agent ingested. Acid ingestion resulted in severe gastritis, which eventually led to antral stenosis and gastric outlet obstruction requiring operative intervention in two cases. Potassium hydroxide capsules produced diffuse esophagitis, gastritis, and a non-healing large gastric ulcer. Clinitest tablets produced distal esophagitis and stricture and antral damage leading to gastric outlet obstruction which required operative intervention. These cases demonstrate the natural history of corrosive injury to the stomach and the value of fiberoptic endoscopy in the management of this problem.
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PMID:Corrosive injury to the stomach: the natural history and role of fiberoptic endoscopy. 45 76

The absorption of carbenoxolone sodium has been studied in 15 patients with gastric ulcer and eight patients with duodenal ulcer treated for four weeks. Blood levels of carbenoxolone showed a log distribution, varied markedly between patients, and were significantly higher after Biogastrone tablets (300 mg/day) than after Duogastrone capsules (200 mg/day). Serum carbenoxolone levels were similar in patients taking Biogastrone tablets before or after meals, and in patients taking Biogastrone tablets or Duogastrone capsules with or without antacids following chronic administration. Serum carbenoxolone levels were similar in patients whose gastric ulcers had or had not healed after four weeks' treatment. Serum carbenoxolone was significantly higher in patients who developed oedema, and was significantly correlated with age and with fall in plasma potassium. Carbenoxolone may exert its metabolic effects systemically, but its ulcer-healing effects topically; additional studies are needed to test this hypothesis.
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PMID:Serum carbenoxolone in patients with gastric and duodenal ulcer: Absorption, efficacy and side-effects. 64 39

Sixty patients with benign chronic gastric ulcer were treated in a controlled clinical trial to assess the relative efficacy of cimetidine and tri-potassium di-citrato bismuthate (De-Nol). Patients were assigned at random either to cimetidine or to De-Nol treatment after initial endoscopic diagnosis. Healing was assessed endoscopically after six weeks by an endoscopist who had no knowledge of the patients' treatment. Consumption of analgesic preparations (both for medical and for non-medical reasons), of other anti-inflammatory agents, and of alcohol and cigarettes was recorded. Of the 57 patients who were reassessed at six weeks, 30 had been assigned to De-Nol and 20 of these patients (66%) had completely healed; 27 patients had been assigned to cimetidine and 17 of these (63%) had also completely healed. Those patients who regularly ingested more than four analgesic preparations a day healed less frequently, but this effect was not statistically significant. There was no significant difference between cimetidine and De-Nol in the initial healing of chronic gastric ulceration. The choice of therapy for chronic gastric ulceration will depend on cost, patient acceptance, and data from studies of more complex therapeutic regimens.
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PMID:Efficacy of cimetidine and tri-potassium di-citrato bismuthate (De-Nol) in chronic gastric ulceration: a comparative study. 76 84

Carbenoxolone sodium has been shown to accelerate the rate of healing of both gastric and duodenal ulcers, but its overall value in duodenal ulcer is probably less because of the high rate of natural remission of duodenal ulcers. Further studies are required to decide whether it should be used prophylactically to delay ulcer recurrence. Carbenoxolone may act by affecting both the proliferative activity of gastric epithelium and the differentiation of the epithelial cells to produce mucus (as well as favourably altering the physicochemical properties of mucus and by reducing peptic activity), factors which may be relevant ot the prevention of acute gastric ulcers. Some studies suggest that carbenoxolone adds to the effect of hospitalisation and bed rest on ulcer healing. Whether bed rest confers additional benefit to the drug's ulcer healing effect in outpatients is also uncertain. There is no evidence that accelerated healing by carbenoxolone is associated with improved overall prognosis. Carbenoxolone is of greatest benefit in accelerating the healing of gastric ulcers in patients for whom hospitalisation is not possible or desirable, but it should only be used in the ambulatory patient when careful and regular observation of serum electrolytes (particularly potassium), blood pressure and weight is possible and when it is known that the patient will attend regular follow-up. Patient must be educated in the proper use of the drug. If severe mineralocorticoid-like toxic effects such as sodium and water retention and hypokalaemia appear, as they do in a variable proportion of patients but most frequently in those receiving excessive doses, carbenoxolone should be stopped and the complication treated; they respond to thiazide diuretics and potassium supplements, and probably to amiloride given in conjunction with a low dose of a thiazide diuretic. Treatment with carbenoxolone can continue with concurrent diuretic therapy in patients with less severe side-effects. Optimum therapeutic effect in gastric ulcer with the least side-effects is achieved with a dosage of 100mg carbenoxolone tablets 3 times daily for the first week followed by 50mg 3 times daily thereafter, best taken before meals. A lower dosage is desirable in the elderly and in those with liver, cardiac or renal disease. Barium meal or preferably endoscopic examinations should be performed regularly and therapy continued until the ulcer is healed. Dosage for duodenal ulcer is 50mg 4 times daily, in special positioned-release capsules. These are best taken about 20 minutes before meals.
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PMID:Carbenoxolone: a review of its pharmacological properties and therapeutic efficacy in peptic ulcer disease. 78 88

The authors present the results of treatment with acetazolamide of gastroduodenal ulcer (356 gastric ulcer, 1.250 duodenal ulcers--859 with craters--, 24 pyloric stenosi with functional components, and 42 postgastrectomy peptic ulcers). The acetazolamide was administed in daily dosis of 25-30 mg/kg of body weight, sodium and potassium salts were added, and the liquid intake was increased (approx. 2 1 daily). A control was kept of the clinical, secretory, radiological, enzymological, and hydrolectrolytical modification. A decrease is observed of the in the carbonic anhidrase of the gastric mucosa and of the gastric secretion. There is also an increase in the gastric protection factors and a disappearance of ulcer pain. There are no significant hydroelectrolytic modifications of the blood. From a radiogical point of view, the crater of the postoperative gastric, pyloric and peptic ulcer disappears after 2 weeks of treatment, and in duodenal ulcers in 89% of the cases in 3 weeks. The method is the same time a quick, simple, an efficient therapeutic test for the differentiation of the gastric craters. The drug is well tolerated. Nevertheless a clinical, secretory and radiological control of the patients is necessary taking into account the counter-indication for the administration of acetazolamide.
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PMID:[Carbonic anhydrase inhibitors in the treatment of gastro-duodenal ulcer]. 82 86

Recognising the inhibitory activity of acetazolamide upon acid gastric secretion and its favorable effects in the treatment of gastric ulcer which we have described (see reference) - we applied the therapeutical testing by acetazolamide in the differentiation of benign from malignant niches of the stomach. Acetazolamide was administered orally at doses of 25-30 mg per kilogram body weight in a long term trial, together with 3 gr sodium bicarbonate, 1 gr potassium bicarbonate, 1.5 gr magnesium oxide per day and an increased quantity of liquids, to 741 patients with radiologically demonstrated ulcer craters. The fundamental criterion was the size of the niche as established by radiologic examination. In all gastric ulcers the size of the niche was considerably reduced after 7-9 days of treatment with acetazolamide; the niche disappeared in 2-3 weeks. This favorable result was obtained without diet and rest. In 38 cases in which there was no significant radiologic change of the niche after 7-9 days of treatment with acetazolamide - the malignancy of the niche was confirmed. The simplicity and the effectiveness of this rapid therapeutic test, makes it useful in the differentiation of benign from a malignant ulcer craters.
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PMID:Therapeutic testing by acetazolamide in the differentiation of a benign from a malignant niche. 88 70

The inhibitory effect of omeprazole on acid formation has been studied in vitro in gastric glands and partly purified H+,K+-ATPase, prepared from mucosa obtained either from healthy subjects by gastroscopic biopsy or from gastric ulcer patients during antrectomy. The effect of omeprazole was compared with the inhibitory pattern of the H2-antagonist cimetidine. Acid production in the glands was determined by measuring the accumulation of 14C-aminopyrine. In glands isolated from patients, omeprazole inhibited acid production maximally stimulated by histamine, db-cAMP, and potassium in a dose-dependent manner, with an IC50 value of about 50 nM irrespective of the agonist used. In contrast, cimetidine inhibited only histamine-induced aminopyrine accumulation, with an IC50 of about 30 micron. The inhibitory effect of omeprazole in db-cAMP-stimulated glands from healthy volunteers was of the same magnitude as seen in glands from gastric ulcer patients. Basal aminopyrine accumulation in glands from both patients and healthy volunteers was almost totally inhibited by omeprazole, whereas cimetidine was without effect. Omeprazole also concentration-dependently inhibited the H+,K+-ATPase activity in isolated gastric membrane vesicles. The estimated IC50 value was 4 micron.
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PMID:Inhibitory action of omeprazole on acid formation in gastric glands and on H+,K+-ATPase isolated from human gastric mucosa. 301 68

The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of omeprazole are reviewed. Omeprazole, a substituted benzimidazole, has a unique site and mechanism of action because it inhibits the proton pump--i.e., hydrogen, potassium adenosine triphosphatase (H+,K+-ATPase)--and consequently blocks the final common step in the gastric acid secretory pathway. Omeprazole inhibits basal and histamine-, gastrin- and pentagastrin-stimulated gastric hydrochloric acid secretion. It produces a dose-dependent reduction in gastric acidity, gastric acid output, and gastric juice volume and has variable effects on pepsin secretion. Omeprazole has no documented effect on esophageal motility or lower esophageal sphincter pressure. Omeprazole is variably absorbed from the gastrointestinal tract, and food appears to decrease the rate, but not the extent, of drug absorption. The drug is approximately 95% bound to plasma proteins and is metabolized to inactive components that are enterohepatically or renally eliminated. Omeprazole is more effective (in most studies) than H2-receptor antagonists in treating duodenal ulcer, at least as effective in treating benign gastric ulcer, and more effective in treating reflux esophagitis. Omeprazole has been used successfully in patients with Zollinger-Ellison syndrome refractory to treatment with H2-receptor antagonists. Gastrointestinal complaints (nausea and diarrhea) are the most commonly reported adverse effects associated with omeprazole therapy. The most frequently reported laboratory abnormality occurring with omeprazole use is elevation of serum aspartate aminotransferase and alanine aminotransferase concentrations. Omeprazole will serve a valuable role in the management of gastrointestinal tract ulcers and hypersecretory conditions.
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PMID:Therapeutic evaluation of omeprazole. 306 85


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