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 aim of the present investigation was to study the efficacy and safety of famotidine (MK-208), a new, potent, histamine H2 receptor antagonist, in promoting the healing of active gastric ulcer when compared to placebo. Of the 71 patients who took part in this multicenter double-blind study in Italy, 37 were administered famotidine 40 mg once daily and 34 placebo. Treatment duration was for up to 8 weeks, and endoscopic and clinical studies were performed at onset and week 4 and, if necessary, at weeks 6 and 8. All patients were carefully evaluated at regular intervals for adverse drug reactions by clinical and laboratory examinations. By the end of the study, 97% of the ulcers were healed in the famotidine group compared to 66% in the placebo group (p less than 0.01). Day and night pain decreased significantly more in the famotidine group than in the placebo group. Both treatments were well tolerated, and no alterations in laboratory tests were observed. Famotidine, therefore, proved effective in the treatment of gastric ulcer and was well tolerated on a short-term basis.
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PMID:Famotidine (MK-208) in the treatment of gastric ulcer. Results of a multicenter double-blind controlled study. 286 35

The epidemiology, pathophysiology, diagnosis, clinical presentation, and treatment of peptic ulcer disease (PUD) are reviewed. PUD occurs commonly, with about 4 million Americans affected in a year. Cigarette smoking, aspirin use, and prolonged corticosteroid use are associated with PUD. The disease's etiology is multifactorial; the long-held assumption that ulcers develop solely because of increased gastric acid secretion is no longer valid. Although duodenal ulcer patients are frequently hypersecretors of acid, gastric ulcer patients more commonly have defective mechanisms for protecting the mucosal lining from acid, pepsin, and other agents. PUD is best diagnosed using an upper gastrointestinal roentgenographic series or using endoscopy. The clinical presentations, which involve epigastric abdominal pain that is relieved by food, milk, or antacids, may aid in diagnosis but are not usually definitive. Treatment is designed to relieve symptoms, heal the ulcer, prevent recurrences, and prevent complications. Of the four currently available drug treatments (cimetidine, ranitidine, antacids, and sucralfate), the treatment of first choice is cimetidine or ranitidine for four or six weeks, respectively, for duodenal and gastric ulcer patients. Antacids should be used as needed for pain, and the patient should be reassessed at the end of this period. For most patients, neither cimetidine nor ranitidine is demonstrably superior to one another. Several agents are under investigation in the U.S., including other H2-receptor antagonists (famotidine and nizatidine), proton-pump inhibitors (omeprazole), prostaglandins (misoprostol, arbasprostil, enprostil, and trimoprostil), antimuscarinic agents (pirenzepine), and tricyclic antidepressants (doxepin and trimipramine). peptic ulcer disease is an important disease. It is best treated with H2-receptor antagonists supplemented with antacids as needed for pain.
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PMID:Current concepts in clinical therapeutics: peptic ulcer disease. 286 52

Two hundred and seventy five patients from six countries were randomized into an endoscopically controlled, eight-week, double-blind, study. The objective of this investigation was to compare the efficacy and safety of nizatidine, administered as either a single (300 mg nocte) or twice daily (150 mg B.D.) dose, with ranitidine 150 mg twice daily, in the therapy of benign gastric ulceration. Two hundred and fifty-two patients fulfilled entry criteria and completed the protocol (80 nizatidine 150 mg B.D.; 89 nizatidine 300 mg nocte; 83 ranitidine 150 mg B.D.). Endoscopy was performed on entry and at four-week intervals until the ulcer healed. The diagnosis of benign ulceration was always supported by endoscopic histology and/or cytology. On entry into the study, both groups appeared well matched (i.e. for population demographics, duodenal ulcer history, previous therapy and pre-study symptomatology), except for epigastric day pain which was significantly less in the ranitidine group (p = 0.020). Overall gastric ulcer healing rates were similar in the three groups at four weeks (nizatidine B.D. 66.2%: nizatidine nocte 65.2%: ranitidine B.D. 63%) and at eight weeks (nizatidine B.D. 90%: nizatidine nocte 86.5%: ranitidine B.D. 86.7%). Healing was not consistently influenced by country of origin or smoking. After four weeks of therapy, 66% (nocte dose) to 68% (B.D. dose) of nizatidine treated patients were symptom free, while 93% (nocte dose) to 95% (B.D. dose) were free of night pain. Events were similar in the three treatment groups, and the majority were gastro-intestinal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nizatidine versus ranitidine in gastric ulcer disease. A European multicentre trial. 289 58

In 363 outpatients with endoscopically confirmed gastric ulcers the efficacy and safety of roxatidine acetate 150 mg at night was compared to 75 mg twice daily. After 8 weeks' treatment substantial reductions in gastric ulcer diameter were obtained in addition to healing rates of 83.7 and 86% for the twice daily and night-time dosing, respectively. Daily reductions in day and night-time epigastric pain were obtained with no significant differences between treatment groups for pain scores or antacid tablet consumption. Furthermore, cigarette smoking did not influence the healing rates produced by either treatment schedule. 26 patients reported 32 adverse reactions and 5 patients discontinued treatment because of side effects, although only 1 of these was a severe reaction. The present data suggest that a single night-time dose of roxatidine acetate 150 mg is as safe and effective as the twice daily dose regimen for the management of acute gastric ulceration.
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PMID:A comparison of roxatidine acetate 150 mg once daily and 75 mg twice daily in gastric ulcer healing. 290 41

A non-comparative multicentre study of 78 patients with healed gastric ulcers who had received roxatidine acetate was conducted to determine the ulcer recurrence rates during 6 months' maintenance therapy with roxatidine acetate 75 mg at night. Gastric ulcer relapses occurred in 35% of patients, representing a worst possible outcome estimate, with no significant differences between smokers and non-smokers although heavy smoking appeared to increase the rate of relapse. The incidence of epigastric pain did not significantly increase over the duration of therapy and while some patients complained of mild pain at the start of the trial all subjects had endoscopically confirmed healed ulcers. The consumption of antacids for symptom relief was low, reaching an average of 0.75 tablets a day which was insufficient to influence intragastric pH. Continuous poor appetite and pyrosis were reported by about 5% of subjects. Of 2 patients who complained of mild to moderate side effects, 1 discontinued treatment. In addition, there were no clinically significant changes in haematological and biochemical variables. Thus, maintenance therapy with roxatidine acetate 75 mg at night is safe and generally effective in preventing symptomatic relapse.
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PMID:Roxatidine acetate in the long term maintenance of gastric ulcers. 290 42

Forty consecutive African patients found to have duodenogastric bile reflux at endoscopy were studied. Bile reflux was found more commonly among males than females, giving a male/female ratio of 2.3:1, with a peak age at 41-60 years. ABO blood groups had no significant influence on duodenogastric bile reflux. Flatulence and borborygmi were the most consistent symptoms other than the classical dyspeptic pain pattern. Bilious vomiting was a rare finding. Duodenogastric bile reflux was more commonly associated with endoscopic gastritis (67.5%), gastric ulcer (35%) and oesophagitis (30%) than with duodenal ulcer (22.5%), deformed pyloric ring (5%) or distorted duodenal bulb (2.5%). The dysfunction in the pyloric sphincter in people with duodenogastric bile reflux appears to be more of a physiological defect than structural.
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PMID:The clinical pattern of duodenogastric bile reflux in the Kenyan Africans. 291 97

Analysis of clinical data obtained in a double-blind randomized study, which compared liquid antacid (neutralizing capacity 120 mmol per day) with 1 g cimetidine in the treatment of 125 patients with gastric ulcer, revealed that, before starting treatment, 71% of the patients complained of epigastric pain, approximately 50% of bloating, and approximately 30% of nausea, heartburn, constipation or vomiting. Epigastric pain before treatment was significantly more frequent in patients with large ulcers (P less than 0.05) and in patients with ulcers unhealed after 4 weeks of therapy (P less than 0.05). This finding was the result of a highly significant correlation between diurnal epigastric pain and ulcer size and delayed healing (P less than 0.005). Nocturnal pain did not correlate with prognosis. In contrast to this correlation between pain before therapy and healing, the disappearance of epigastric pain with therapy did not signify ulcer healing. Only 14 (38%) of the 37 patients with healed ulcer were free from pain after the 4 weeks of therapy, whereas 25 (49%) of the 52 patients with persistent ulcers had no pain at this time. Placebo pain tablets relieved ulcer pain effectively in more than 85% of the patients, irrespective of whether the ulcer was healing or not. The other symptoms (bloating, nausea, heartburn, constipation or vomiting) were also alleviated by 4 weeks of therapy but no correlation was found with ulcer size or prognosis. The loss of the prognostic significance of ulcer pain is probably due to a complex interaction of the trial schedule on the patient's level of consciousness.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Loss of predictive value of gastric ulcer symptoms in a randomized treatment trial. 297 76

In a multi-centre double-blind (double-dummy) trial the effectiveness of low-dose antacid gel (6 X 12 ml/d; neutralisation capacity 120 mmol) was compared with that of a standard dose of cimetidine (1 g/d) in the curative treatment of gastric ulcer. Antacid gel was given to 65 patients, cimetidine to 60. Diagnosis was confirmed by endoscopic biopsy, which was also employed in a serial follow-up. After 4 weeks antacid gel and cimetidine produced cures in 43% and 52%, respectively; after 8 weeks 76% and 89%, respectively, the difference between the two methods not being statistically significant. There was also no statistically significant difference with regard to ulcer pain. In one case each in the antacid and cimetidine groups, the treatment had to be stopped because of side effects. Diarrhoea was more common on cimetidine than on antacid gel. It is concluded that both low-dose antacids gels and cimetidine are suitable in the treatment of gastric ulcers.
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PMID:[Therapy of stomach ulcer with low-dose antacid gel and cimetidine. A multicenter double-blind study]. 298 63

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

The fact that nonsteroidal anti-inflammatory drugs (NSAIDs) damage the gastroduodenal mucosa is no longer contested. Endoscopic studies in normal volunteers after NSAID administration have failed to predict which NSAIDs would be safest when administered chronically. NSAID use has been associated with a disproportionately high frequency of upper gastrointestinal bleeding and perforation of ulcers. All of the newer NSAIDs appear to be similar in their propensity to cause mucosal damage, including peptic ulceration. On any given day, more than 10% of patients receiving NSAIDs chronically will have a gastric ulcer, a point prevalence of ulcer disease at least 5 to 10 times higher than in patients who are not taking NSAIDs. The dose-response relationship between anti-inflammatory activity and untoward events, coupled with increased use of newer more potent NSAIDs, explains, in part, the increased incidence of NSAID-associated ulcer complication of bleeding and perforation. The possible association of the increase in prevalence of Campylobacter pylori gastritis with aging and the apparent increase in NSAID-associated complications in the elderly is discussed. The current status of nonsteroidal drug therapy can be summarized as follows: 1) new NSAIDs are not safer than the old NSAIDs, as far as major gastrointestinal side effects are concerned, 2) NSAIDs should be avoided when analgesia is the main goal, 3) if NSAIDs are required, the lowest possible dose that achieves pain relief should be used, 4) newer NSAIDs available only in relatively high anti-inflammatory activity dosages should be restricted to those patients in whom high levels of anti-inflammatory activity are desired.
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PMID:Gastroduodenal complications of chronic NSAID therapy. 304 80


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