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)

Risk factors of slow healing were previously researched in a large sample of duodenal (DU) and gastric ulcer (GU) patients over 65 years of age; persistence of ulcer symptoms was proven the most reliable factor in predicting nonhealing ulcer, while ulcer size was of importance only for DU. We aimed to complete the analysis, with a more careful evaluation of concomitant diseases and therapies. Ranitidine 300 mg daily was given for four to eight weeks to 310 GU and 699 DU patients. Ninety-three patients dropped out of the study; 79/294 gastric ulcers and 138/635 duodenal ulcers were unhealed after four weeks. Cardiovascular, gastrointestinal, and pulmonary disorders were the most frequent concomitant diseases; NSAIDs, cardiovascular drugs, and antihypertensives were the most frequent concomitant therapies. Esophagitis was diagnosed in 15.5% of patients. Ulcer healing was the major determinant of persistence of ulcer symptoms; esophagitis emerged as an important adjunctive and independent factor. Use of hypoglycemic agents in the whole sample and smoking habit (in GU) may have also a role. With persistence of ulcer symptoms removed from the analysis, ulcer size was the most constant factor affecting ulcer healing. NSAID use, cardiovascular disorders, esophagitis (in GU), and concomitant therapy with cardiovascular drugs (in DU) also play a role. In conclusion, persistence of ulcer symptoms, the major indicator of slow ulcer healing in the elderly, is independently affected also by the presence of esophagitis. Use of hypoglycemic agents and smoking habit may also have a role in persistence of ulcer symptoms. NSAIDs, cardiovascular disorders, cardiovascular drugs, and esophagitis affect ulcer healing, for which the most constant indicators remained persistence of ulcer symptoms and ulcer size.
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PMID:Do concomitant diseases and therapies affect the persistence of ulcer symptoms in the elderly? 856 52

As many as 89% of gastric ulcer patients experience ulcer recurrences within 1 year of successful healing with conventional antiulcer therapies. Because ranitidine is effective in the healing of gastric and duodenal ulcers and the maintenance of healed duodenal ulcers, we hypothesized that ranitidine would also be effective in the maintenance of healed gastric ulcers. A 48-week, placebo-controlled, randomized, double-blind, multicenter trial was conducted to compare ranitidine 150 mg administered at bedtime with placebo for the maintenance of healed gastric ulcers. Endoscopies were performed at baseline and repeated after 12, 24, 36, and 48 weeks of treatment. Gastric ulcer recurrence rates at each scheduled endoscopy were significantly lower in patients receiving ranitidine (5%, 13%, 16%, and 19%, respectively) compared with those receiving placebo (20%, 30%, 40%, and 50%, respectively). Compared with placebo, ranitidine was more effective in maintaining healed gastric ulcers regardless of previous gastric ulcer history, smoking status, age (< 65 vs > or = 65 years), or sex. There were no significant differences between the two treatment groups in the number of patients experiencing adverse events or laboratory abnormalities. Ranitidine 150 mg administered at bedtime provides safe and effective treatment for the maintenance of healed gastric ulcers.
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PMID:Effectiveness of ranitidine 150 mg at bedtime as maintenance therapy for healed gastric ulcers. 900 34

The authors studied ranitidine effects on the function of glucocorticoid receptors (GR) of gastric cytosol in patients with massive bleeding from gastric ulcer. Fast cytosol was obtained from the tissues taken from the great culvature of the resected stomach. GR type II and III were identified using 3H-acetonide triamcinolone and 3H-hydrocortisone with high specific activity, respectively. Ranitidine (10(-3) and 10(-2) M) effects on the function of GR type II and III were analyzed according to Scatchard. Ranitidine (10(-2) M) increased 4 times the number of sites of glucocorticoid receptor binding for acetonide triamcinolone and aroused the association constant of hormone-receptor complex. Ranitidine dose-dependently reduced the number of binding sites of GR type III for hydrocortisone. Thus, ranitidine modulates type II and III GR function.
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PMID:[Effect of ranitidine on the function of the gastric glucocorticoid receptors]. 947 94

A total of 1,456 patients were available for the All Patients Treated analysis of two large, randomized, double-blind, multicenter, controlled studies (Acid Suppression Trial: Ranitidine versus Omeprazole for NSAID-Associated Ulcer Treatment [ASTRONAUT] and Omeprazole versus Misoprostol for NSAID-Induced Ulcer Management [OMNIUM]). These studies examined the efficacies of omeprazole, 20 and 40 mg once daily (both studies), ranitidine, 150 mg twice daily (ASTRONAUT), and misoprostol, 200 microg four times daily (OMNIUM), for the healing of gastric ulcer, duodenal ulcer, or erosions, and the relief of dyspeptic symptoms. At entry, patients were receiving, and continued to receive, nonsteroidal anti-inflammatory drugs (NSAIDs), and had a gastric or duodenal ulcer, and/or >10 erosions in the stomach or duodenum at initial endoscopy. Patients were randomized to blinded treatment for 4/8 weeks until treatment success, which was defined as the healing of ulcer(s), <5 erosions at any site, and not more than mild dyspeptic symptoms. The proportions of patients reaching treatment success by 8 weeks were 77% with both doses of omeprazole, 63% with ranitidine, and 71% with misoprostol. In patients who initially had a gastric ulcer, more ulcers were healed at 8 weeks with omeprazole, 20 (83%) and 40 mg once daily (82%), than with ranitidine (64%) or misoprostol (74%). In patients who initially had a duodenal ulcer, 93% were healed at 8 weeks with omeprazole, 20 mg once daily, compared with 88% for omeprazole, 40 mg once daily, 79% for ranitidine, and 79% for misoprostol. Erosions healed slightly faster at 4 weeks with misoprostol, compared with the other regimens, but by 8 weeks most patients had <5 erosions per gastroduodenal region in each treatment group. Diarrhea and abdominal pain were more common in patients taking misoprostol, as were adverse events leading to withdrawal. Patients with duodenal ulcer or erosions at entry and the presence of Helicobacter pylori were good prognostic factors for overall treatment success. Using a model that included only patients with ulcers, those with smaller ulcers also had a higher likelihood of achieving treatment success. Against the background of these new data, omeprazole is the treatment of choice for healing NSAID-associated ulcers, on the basis of its efficacy and tolerability, and the optimal dose appears to be 20 mg once daily.
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PMID:New data on healing of nonsteroidal anti-inflammatory drug-associated ulcers and erosions. Omeprazole NSAID Steering Committee. 957 22

Four large clinical studies have shown that omeprazole, 20 mg once daily, is effective in preventing the significant gastroduodenal consequences of nonsteroidal anti-inflammatory drugs (NSAIDs). In the Scandinavian Collaborative Ulcer Recurrence (SCUR) study, patients were randomized (without initial endoscopy) to receive omeprazole or placebo for up to 3 months. Of the patients treated with omeprazole, 24.7% experienced treatment failure, compared with 50.0% of those on placebo. Fewer patients in the omeprazole group than in the placebo group developed a peptic ulcer (4.7% versus 16.7%, respectively) or dyspeptic symptoms (8.2% versus 20.0%, respectively). In the Omeprazole versus Placebo as Prophylaxis of Ulcers and Erosions from NSAID Treatment (OPPULENT) study, patients were also randomized to receive omeprazole or placebo. The estimated probability of remaining in remission for 6 months while receiving omeprazole was 0.78, compared with 0.53 for placebo. Fourteen (16.5%) patients on placebo developed peptic ulcer(s), compared with three (3.6%) patients on omeprazole. The Omeprazole versus Misoprostol for NSAID-Induced Ulcer Management (OMNIUM) study consisted of a healing and a prophylactic phase. Patients who successfully completed the healing phase were re-randomized to receive omeprazole, misoprostol, or placebo for up to 6 months. In patients receiving omeprazole, 36.5% experienced treatment failure, compared with 48.6% of those on misoprostol, and 67.7% of those on placebo. Omeprazole and misoprostol appeared to be equally effective in preventing gastric ulcer; by contrast, omeprazole was highly effective in preventing duodenal ulcer, when compared with misoprostol and placebo. The Acid Suppression Trial: Ranitidine versus Omeprazole for NSAID-Associated Ulcer Treatment (ASTRONAUT) study also consisted of a healing and a prophylactic phase. Patients who successfully completed the healing phase were re-randomized to receive omeprazole or ranitidine for up to 6 months. In patients receiving omeprazole, 26.2% experienced treatment failure, compared with 37.7% of those on ranitidine. The percentages of patients with a peptic ulcer relapse were 5.7% for omeprazole and 19.5% for ranitidine. The data show that omeprazole is an effective and well-tolerated agent for both primary and secondary (maintenance) prophylaxis in patients receiving NSAIDs.
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PMID:Progress in prophylaxis against nonsteroidal anti-inflammatory drug-associated ulcers and erosions. Omeprazole NSAID Steering Committee. 957 24

The pharmacological profile of N-[3-[2-[N'-(2-methoxyethyl)guanidino]thiazol-4yl]benzyl-ace tamide (FR145715), a novel histamine H2 receptor antagonist, was examined in both in vitro and in vivo models using experimental animals in comparison with ranitidine. In isolated guinea-pig atria, FR145715 antagonized the effect of histamine on heart rate with approximately three times more potent activity than ranitidine. In in vivo experiments, intraduodenal FR145715 dose-dependently inhibited spontaneous gastric acid secretion in rats (Shay's rats), with a ED50 value of 18.4 mg/kg, which was comparable to that of ranitidine (30.5 mg/kg). FR145715 also inhibited histamine-stimulated acid secretion in stomach-perfused anaesthetized rats (Schild's rats), when given intravenously and intraduodenally with ED50 values of 0.59 and 2.72 mg/kg, respectively. Ranitidine displayed more potent activity having respective ED50 values of 0.10 and 0.17 mg/kg. In Heidenhain pouch dogs, intravenous and oral FR145715 dose-dependently inhibited gastrin-stimulated acid secretion with respective ED50 values of 0.12 and 0.32 mg/kg, which were similar to those of ranitidine (0.09 and 0.33 mg/kg). In gastric ulcer models, FR145715 dose-dependently inhibited water immersion restraint stress- and acidified aspirin-induced gastric lesions with ED50 values of 3.2 and 15.1 mg/kg (p.o.), respectively. The comparative compound, ranitidine, also showed beneficial effects on stress-induced gastric ulcers with an ED50 value of 1.5 mg/kg (p.o.). However, it failed to inhibit acidified aspirin-induced gastric ulcers. FR145715 inhibited HCl-induced gastric lesions in rats, while pre-treatment with indomethacin abolished its beneficial effects, suggesting that FR145715 has a so-called cytoprotective effect which is dependent on endogenous prostaglandin production. In addition to its atypical profile as a histamine H2 receptor antagonist, FR145715 exhibited strong anti-microbial activities against strains of Helicobacter pylori (H. pylori) with a mean minimal inhibitory concentration value of 0.32 microg/ml. Moreover, FR145715 showed no anti-microbial effects on 25 other bacteria examined. In addition, in vivo experiments using gnotobiotic piglets infected with H. pylori, FR145715 (16 mg/kg, t.i.d.) completely eliminated the organism with reduced intensity of inflammation, when treated orally for 10 days. These data demonstrate that FR145715 is a novel histamine H2 receptor antagonist having potent and selective anti-H. pylori activities as well as cytoprotective properties. The present data suggest that FR145715 might be useful for the patients suffering from ulcer relapse, since the drug might be able to eradicate H. pylori in the stomach, which is considered a key factor to cause ulcer recurrence in humans.
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PMID:FR145715, a novel histamine H2 receptor antagonist, with specific anti-Helicobacter pylori activities. 1049 6

The use of H2-blockers in the treatment of patients with peptic ulcer has become popular. However, this treatment has adverse cardiovascular effects. The aim of this study was to investigate proarrhythmic rhythm and autonomic nervous activity by analyzing heart rate variability in patients treated with omeprazole, ranitidine, and plaunotol. Nineteen patients (mean age 67.5 +/- 2.7 years) with active gastric ulcer were treated with omeprazole (20 mg/day) for 8 weeks, then ranitidine (300 mg/day) for the next 4 months, and finally plaunotol (240 mg/day). At each stage of the treatment, Holter electrocardiography was performed, and heart rate variability and arrhythmias analyzed. Heart rate variability yielded power in the low- (0.04-0.15 Hz) and high-frequency components (0.15-0.4 Hz). Although both ranitidine and omeprazole induced little change in cardiac rhythm, the high-frequency power was higher (10.3 +/- 0.8 vs 8.6 +/- 0.6 ms, P < 0.05) and the ratio of low-to-high frequency power was lower (1.41 +/-0.10 vs 1.59 +/- 0.09. P < 0.05) during ranitidine than during plaunotol treatment. Cosinor analysis of heart rate variability revealed a decreased amplitude of low-frequency power during omeprazole compared with during ranitidine and plaunotol treatment. Ranitidine modulated high-frequency power which may be related to the adverse cardiovascular effects of H2-blocker.
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PMID:H2-blocker modulates heart rate variability. 1077 6

Two recently reported studies of nonsteroidal anti-inflammatory drugs (NSAIDs), the Omeprazole versus Misoprostol for NSAID-induced Ulcer Management and the Acid Suppression Trial: Ranitidine versus Omeprazole for NSAID-associated Ulcer Treatment studies, concluded that omeprazole was superior to a subtherapeutic misoprostol or an ineffective dose of ranitidine for the endpoint, prevention of gastroduodenal ulcers in chronic NSAID users. Helicobacter pylori status was collected prospectively but was not reported. We report separate analyses for patients with unequivocal NSAID ulcers (H. pylori negative) and patients whose NSAID use was complicated by the presence of an active H. pylori infection. Omeprazole was superior to placebo for the prevention of ulcer recurrence in chronic NSAID users. However, omeprazole was not significantly better than a subtherapeutic dose of misoprostol for the prevention of gastroduodenal ulcers in chronic NSAID users. Misoprostol was superior to omeprazole for the prevention of gastric ulcers among those patients with unequivocal NSAID ulcers (8.2% vs 16.6%, respectively; P <0.05). Omeprazole was not statistically different from misoprostol for gastric ulcer prevention in those whose NSAID use was complicated by an active H. pylori infection. Ranitidine and omeprazole were also not statistically different for the prevention of unequivocal NSAID gastric ulcers (14.6% vs 11.6%, respectively; P = 0.56). That the Misoprostol Ulcer Complications Outcomes Safety Assessment (MUCOSA) trial found full-dose misoprostol to be more effective in ulcer prevention than it was in prevention of ulcer complications suggests that either many of the ulcer complications were related to H. pylori ulcers or that more antisecretory activity than can be provided with misoprostol is needed, or both. The question remains whether the combination of low-dose misoprostol plus an antisecretory drug (either an H(2)-receptor antagonist or a proton pump inhibitor) would provide superior results compared with either alone. That omeprazole was not superior to one half the dose of misoprostol used in the ulcer complication prevention, or MUCOSA, study indicates that it would not be prudent to suggest that ulcer prevention with omeprazole alone would be able to provide similar protection to misoprostol.
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PMID:Helicobacter pylori and nonsteroidal anti-inflammatory drugs: interaction with proton pump inhibitor therapy for prevention of nonsteroidal anti-inflammatory drug ulcers and ulcer complications--future research needs. 1116

The frequency, symptoms, and complication rate of PUD seem to decrease during pregnancy. Yet clinicians often have to treat dyspepsia or pyrosis of undetermined origin during pregnancy because the frequency of pyrosis significantly increases during pregnancy, and clinicians reluctantly perform EGD during pregnancy for pyrosis to differentiate reliably between GERD and PUD. Dyspepsia or pyrosis during pregnancy is initially treated with dietary and lifestyle modifications. If the symptoms do not remit with these modifications, sucralfate or antacids, preferably magnesium-containing or aluminum-containing antacids, should be administered. Histamine2 receptor antagonists are recommended when symptoms are refractory to antacid or sucralfate therapy. Ranitidine seems to be a relatively safe H2 receptor antagonist. If symptoms continue despite H2 receptor antagonist therapy, the patient should be evaluated for possible EGD or PPI therapy. Pregnant women with hemodynamically significant upper gastrointestinal bleeding or other worrisome clinical findings should undergo EGD. Indications for surgery include ulcer perforation, ongoing active bleeding from an ulcer requiring transfusion of six or more units of packed erythrocytes, gastric outlet obstruction refractory to intense medical therapy, and a malignant gastric ulcer without evident metastases.
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PMID:Gastric and duodenal ulcers during pregnancy. 1263 19

The present study was designed to investigate the effect of Mimusops elengi (Sapotaceae) against experimental gastric ulcers. The 50% alcoholic extract of Mimusops elengi (Ext E) and its different fractions namely ethyl acetate (Ext E1), n-butanol (Ext E2), methanol (Ext E3) and aqueous (Ext E4) were studied (p.o.) against ethanol-induced gastric damage. Ext E1 was also studied in ethanol-induced, pylorus-ligated and water-immersion plus stress-induced gastric ulcer models. Ranitidine HCl (80 mg kg(-1)) was used as a reference standard. In ethanol-induced gastric ulcer model, pantoprazole (20 mg kg(-1)) was also used as a reference standard. Ext E1 tested in mice up to the dose of 5000 mg kg(-1) (p.o.) did not produce any sign of toxicity. Ext E at the doses of 50, 100, 300 and 500 mg kg(-1) and its different fractions (100 mg kg(-1)) showed reduction in gastric ulceration (P < 0.05). Ext E1 at the doses of 10, 50 and 100 mg kg(-1) showed dose-dependent inhibition of gastric lesions against ethanol-induced gastric damage. In 19 h pylorus-ligated animals, Ext E1 at 50 and 100 mg kg(-1) doses showed significant reduction in ulcer index (P < 0.05). Significant reduction was also observed in total acidity, volume of gastric acid secretion, total acid output and pepsin activity (P < 0.05) when compared with the control group. Besides, Ext E1 showed increase in the mucosal glycoproteins that was evident from significant rise in total carbohydrates to protein ratio (TC:PR ratio) (P < 0.05), which is an indication of mucin activity. Ext E1 also showed protection against water-immersion plus stress-induced gastric lesions that was evident from dose-dependent decrease in ulcer index (P < 0.05), score for intensity (P < 0.05) and total lesion area (P < 0.05) when compared with the control group. It can be concluded from our study that Ext E1 possesses anti-ulcer activity against experimental gastric ulcers. The mechanism of anti-ulcer activity can be attributed to decrease in gastric acid secretory activity along with strengthening of mucosal defensive mechanisms.
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PMID:Study of Mimusops elengi bark in experimental gastric ulcers. 1461 97


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