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 effects of a new H2-receptor antagonist, roxatidine acetate, have been investigated in both clinical and pharmacodynamic trials in Europe and the United States. A series of four double-blind randomized studies are reviewed, reporting the effects of different dose regimens of roxatidine acetate compared with ranitidine and placebo in healthy volunteers using continuous intragastric pH monitoring. These pharmacodynamic studies clearly demonstrate that roxatidine acetate is an effective gastric antisecretory agent, which is up to twice as potent as ranitidine. The results of several clinical studies of roxatidine acetate in patients with gastric as well as duodenal ulcer conducted in Europe, Japan, and the United States are also reviewed. These studies show that roxatidine acetate is comparable to other potent H2-receptor antagonists in terms of cumulative healing rates, pain relief, and safety. Overall, the pharmacodynamic and clinical data indicate that the efficacy of roxatidine acetate 75 mg twice-daily (b.i.d.) does not differ significantly from ranitidine 150 mg b.i.d. Roxatidine acetate is equally effective in the treatment of peptic disease including gastric ulcer, duodenal ulcer, and reflux esophagitis.
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PMID:Safety and efficacy of roxatidine acetate. Evidence from pharmacodynamic and clinical trials. 257 21

Omeprazole inhibits H+,K+-ATPase, the enzyme responsible for the exchange of H+ and K+ in the final step in the acid secretory process within the parietal cell. It has been shown to produce a marked and long-lasting inhibition of acid secretion with a decrease in 24-hour intragastric acidity after repeated daily dosing. Omeprazole has been shown to give significantly higher healing rates than ranitidine or cimetidine in patients with duodenal ulcer and gastric ulcer. Similarly, a more pronounced effect on ulcer symptoms has been observed. In patients with reflux esophagitis, omeprazole has been shown to decrease the time with an acid milieu in the esophagus. Omeprazole has consistently given about twice as high healing rates and faster decrease in symptoms than with ranitidine. In patients with Zollinger-Ellison syndrome, omeprazole has been found to have a rapid and long-lasting effect on acid secretion and acid-induced symptoms.
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PMID:Clinical utility and safety of omeprazole. 265 79

Although the approved indications for long-term histamine (H2) receptor-antagonists are limited to the management of hypersecretory states and prophylaxis against recurrent duodenal ulcer, these agents are often prescribed indiscriminately. Definitive guidelines concerning proper patient selection for prophylaxis against duodenal ulcer recurrence are lacking. Persons likely to benefit from maintenance therapy include those who smoke and those with a long duration of symptoms or prior history of an ulcer complication. Although not an approved indication, maintenance therapy to prevent recurrent gastric ulcer is appropriate for elderly persons receiving nonsteroidal anti-inflammatory drugs or in patients with poor cardiopulmonary status who may not tolerate surgery for an ulcer-related complication. The role of long-term H2-antagonist therapy in reflux esophagitis is not defined but may be appropriate in scleroderma and Barrett's esophagus. Finally, several miscellaneous conditions, including cystic fibrosis, Menetrier's disease, and pancreatic exocrine insufficiency, may benefit from long-term H2-antagonist therapy. Currently, clinical trials document the efficacy of maintenance therapy in duodenal ulcer for up to a three-year period; however, for gastric ulcer and chronic reflux esophagitis, the duration and benefit of long-term therapy is not established, and treatment regimens need to be individualized. Therapy may be required indefinitely in the miscellaneous states mentioned previously.
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PMID:Rational approach to long-term use of H2-antagonists. 288 77

The H+K+-ATPase is supposed to be the terminal step in the acid-secreting pathway in the parietal cell. Omeprazole blocks this enzyme, resulting in a marked inhibition of basal and stimulated acid secretion. With omeprazole 20 mg daily, 24-hour intragastric acidity is decreased by about 90%. Several clinical studies have now been published in which omeprazole has been compared with the H2-receptor antagonists cimetidine and ranitidine. Omeprazole in doses between 20 and 40 mg daily resulted in healing rates between 65% and 82% after treatment for 2 weeks and between 90% and 100% after treatment for 4 weeks. Treatment with omeprazole also gave faster and more pronounced pain relief. One comparative study in gastric ulcer has also been published showing healing rates equal to those with ranitidine. Placebo-controlled trials have also shown very pronounced therapeutic effect in reflux esophagitis. Omeprazole seems to be the drug of choice in Zollinger-Ellison syndrome, giving beneficial clinical effects and pronounced and long-lasting reduction in gastric acid secretion.
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PMID:Clinical perspectives of drugs inhibiting acid secretion--H+K+-ATPase inhibitors. 302 57

Experimentally, the gastric and the duodenal mucosa can both be damaged by acute exposure to small intestinal juice. Though chronic exposure to bile causes mucosal erythema and hyperplasia, the gastric mucosal barrier is not damaged. Duodenogastric reflux is relevant in the pathogenesis of postoperative bilious vomiting and probably of "alkaline" reflux esophagitis. The exact mechanism of mucosal damage has not been established. Duodenogastric reflux is likely to be irrelevant in the pathogenesis of (microscopic) gastritis, of gastric ulcer, and of reflux esophagitis without previous gastric surgery.
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PMID:[Is a duodenogastric reflux of pathogenic significance?]. 305 2

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

Misoprostol was provided on a humanitarian basis to 157 patients with severe, often life-threatening, refractory upper gastrointestinal (UGI) disease not managed by available medical therapy (cimetidine, ranitidine, antacids, sucralfate, and/or prior surgery). A total of 162 separate clinical treatment courses were evaluated in the 157 patients for the period May 1, 1981 to May 6, 1986. Misoprostol was administered orally or via nasogastric tube, 800 micrograms to 1,200 micrograms daily in four to six divided doses, for periods of from one day to 17 months. Patients were considered to have a favorable clinical outcome if they achieved significant improvement in symptoms, hemorrhagic status, or appearance of their condition on endoscopy. Favorable clinical outcomes were observed in 52 of 83 treatment courses (63 percent) involving UGI hemorrhage and in 44 of 79 treatment courses (56 percent) for long-standing nonhemorrhagic UGI disease. A total of 116 treatment courses were for patients with a single UGI entry diagnosis; 28 treatment courses were for patients with two UGI entry diagnoses; four courses were for patients with three UGI entry diagnoses; and 14 treatment courses were for miscellaneous UGI entry diagnoses. Treatment outcomes were analyzed by the four most commonly treated UGI entry diagnoses; patients who had an initial diagnosis of refractory duodenal ulcer (n = 28), refractory gastric ulcer (n = 41), reflux esophagitis (n = 23), or hemorrhagic gastritis (n = 63) had favorable clinical outcomes of 71 percent, 58 percent, 61 percent, and 62 percent, respectively. Misoprostol was well tolerated, with the most common adverse experience being mild to moderate diarrhea. It is concluded that in humanitarian clinical trials, misoprostol was frequently associated with symptomatic relief, with improvement in UGI hemorrhage, or with endoscopic improvement in severe UGI disease that had proven refractory to available medical therapy.
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PMID:Humanitarian use of misoprostol in severe refractory upper gastrointestinal disease. 311 46

The orodental status, particularly dental erosions, of 109 patients with upper gastrointestinal symptoms was examined. In 44 patients, the underlying pathosis was associated with increased acid output in the stomach (reflux esophagitis or duodenal ulcer), while in 48 patients who underwent cholecystectomy, the duodenogastric reflux was alkaline. In 17 patients with gastric ulcer, the gastric secretion was usually normal. The diagnoses were made with gastroscopy. Seven patients with dental erosion were found, and they all came from the group of 35 dental patients with reflux esophagitis or duodenal ulcer. No erosions were seen in the other diagnostic groups (F = 0.02). Thus, gastrointestinal disorders with increased output of gastric acid may be linked with dental erosions. The finding emphasizes the need for accurate diagnosis and appropriate treatment of patients with upper gastrointestinal symptoms in order to avoid irreversible lesions in the teeth.
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PMID:Dental erosion and upper gastrointestinal disorders. 316 79

Bile reflux has been implicated in the pathogenesis of gastritis, gastric ulcer, and esophagitis. Radionuclide techniques provide the only non-invasive method to detect duodenogastric reflux. To analyze the problems that occur with attempts at quantitation, 55 patients were prospectively evaluated (45 patients with reflux esophagitis or Barrett's esophagus and ten patients with clinical symptoms of bile reflux, four of whom had Bilroth II surgery) with Tc-99m DISIDA, using a fasting technique with gallbladder stimulation by sincalide. Visual duodenogastric reflux occurred in 16 of 55 patients. Overlap of small bowel with the stomach is the major problem for accurate quantitation and occurred in 20 of 55 patients (36%). Overlap of left lobe of the liver occurred in 40 of 55 patients (73%), but its contribution to gastric activity was slight and could be easily subtracted. Reflux was intermittent in six of the 16 positive studies (38%), and continuous computer acquisition is needed to detect its maximum value. Primarily because of the problem of small bowel overlap, scintigraphic evaluation of duodenogastric reflux is only, at best, semi-quantitative. A review of the technical variables used in this examination, as well as potential problems that can occur, is provided.
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PMID:Scintigraphic evaluation of duodenogastric reflux. Problems, pitfalls, and technical review. 358 23

Clinical findings, symptoms and predisposing factors were studied in 43 patients with oesophageal candidiasis, 40 patients with peptic oesophagitis and 40 normal controls. Oesophageal candidiasis was confirmed cytologically. 2.4% of patients who had undergone gastroscopy had oesophageal candidiasis; only three of them had simultaneous candidiasis of the oral cavity. Cardiac failure, oesophageal varices, hiatus hernia and gastric ulcer were common associated disorders. 42% of patients with candidal oesophagitis were symptom-free. Most common symptoms were vomiting, retrosternal and epigastric pain. Peptic oesophagitis was more frequently associated with symptoms. Predisposing factors were present in 88% of cases of oesophageal candidiasis: alcoholism, hepatic cirrhosis, diabetes mellitus, malignant tumours and other wasting diseases. 18 patients had had treatment with cimetidine; they included all 13 patients whose candidiasis was first detected at check endoscopy.
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PMID:[Candidiasis of the esophagus. Prospective study of incidence, type of complaints and predisposing factors]. 373 73


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