Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D00446 (Sucralfate)
 278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pharmacologic management of peptic ulcer disease continues to evolve with the introduction of diverse types of new therapeutic agents. The ideal aims of treatment of peptic ulcer disease are to relieve pain, heal the ulcer, and delay ulcer recurrence. This article provides a broad perspective on the pharmacology and therapeutic actions of antiulcer drugs. To date, no drug meets all goals of therapy. Drug treatment of peptic ulcers is targeted at either counteracting aggressive factors or stimulating the mucosal defense. Drugs that inhibit or neutralize gastric acid secretion include histamine H2-receptor antagonists, proton pump inhibitors, anticholinergics, prostaglandins, and antacids. H2-receptor antagonists have become first-line drugs for treatment of uncomplicated duodenal ulcers, gastric ulcers, prevention of ulcer relapse, and mild esophagitis. However, H2-receptor antagonists, like other gastric antisecretory/antiulcer drugs, have high rates of ulcer recurrence following discontinuation of therapy. They therefore need to be administered continuously in patients prone to such recurrences. Omeprazole has emerged as a major drug for the treatment of severe erosive esophagitis, refractory ulcers, and Zollinger-Ellison syndrome. The major disadvantage of proton pump inhibitors is the concern for their long-term safety. The roles of M1-antimuscarinic agents and antacids have not been fully defined. Misoprostol, effective for the treatment of gastric and duodenal ulcers, is now the only drug that prevents ulcers induced by nonsteroidal anti-inflammatory drugs. Mucosal protective drugs that do not inhibit gastric acid secretion include sucralfate and organic bismuth salts. Sucralfate is a nonsystemic, well-tolerated, effective drug for treatment of duodenal ulcers and prevention of duodenal ulcer relapse. The organic bismuth salt bismuth subcitrate is efficacious in the treatment of duodenal and gastric ulcers. Furthermore, it has also been established that it alters the course of ulcer recurrence. However, bismuth encephalopathy is a major toxicity concern that needs to be addressed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Drugs for treatment of peptic ulcers. 135 99

Epidermal growth factor (EGF) has been shown to enhance healing of experimental gastric ulcers when given subcutaneously or orally in the drinking water. This effect of EGF occurs without reducing gastric acid secretion. On the other hand, EGF reportedly is excreted rapidly from gastric lumen when administered by intragastric bolus. This suggests that further stimulation of ulcer healing may be expected if EGF is given with an acid-suppressive agent or with an agent allowing EGF to remain in rat gastric lumen at high concentrations. In the present study, EGF administered by gastric intubation at a dose of 10 micrograms/kg, which is three times smaller than reported in previous studies, was evaluated for its effect on acetic acid-induced rat gastric ulcers in combination with sucralfate or omeprazole. Sucralfate is well known selectively to bind proteins covering the ulcer base, and omeprazole is a potent acid-suppressive agent. Prior to the study of combined EGF and sucralfate, oral sucralfate was confirmed to allow endogenous gastric EGF and mouse EGF given exogenously to remain at high concentrations in gastric contents and tissues. EGF and sucralfate (2 g/kg/day) given alone failed to stimulate ulcer healing in submandibularectomized rats (SMR rat) whose endogenous gastric EGF was depleted. However, the combination of both drugs administered at the same doses significantly accelerated ulcer healing in the SMR rat. Omeprazole (200 mg/kg/day) significantly enhanced ulcer healing regardless of removal of the submandibular glands. The combination of EGF and omeprazole further stimulated ulcer healing in the SMR rat.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of epidermal growth factor in combination with sucralfate or omeprazole on the healing of chronic gastric ulcers in the rat. 221 45

The aim of this study was to analyze the results and the quality of methodology of 51 controlled double blind trials in the medical treatment of gastroesophageal reflux. The results of H2 receptor antagonist treatment were evaluated by the pooling method. Evaluation of methodology was carried out by using a special form filled in by two independent observers. The major criticisms in methodology were: small sample size, unblind evaluation of end-points, inappropriate statistical tests for small samples, and inaccurate handling of the withdrawals. There were only two trials concerning antacids versus placebo: one showed that Novaluzid improved symptoms and another that Maalox did not differ from placebo. The effectiveness of alginic acid and domperidone on either symptoms or endoscopic lesions was not demonstrated. Metoclopramide and bethanechol produced significant relief of reflux symptoms. Sucralfate and bethanechol were better than placebo in improvement of esophagitis endoscopic lesions. The H2-inhibitors efficiently relieved symptoms and esophagitis. Pooling analysis showed that H2-inhibitors were superior to placebo in the healing of esophagitis; the odds ratios were 2.5 for cimetidine and 3.3 for ranitidine, without significant difference. Omeprazole was better than ranitidine in relief of symptoms and esophagitis. The comparison of cimetidine alone with cimetidine plus metoclopramide showed that combined therapy was better in one trial out of two. New controlled trials are necessary to compare these different drugs and their association.
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PMID:[Treatment of gastroesophageal reflux: analysis of randomized double-blind trials]. 289 80

With rare exception, peptic ulcers can now be classified as either Helicobacter pylori-related, induced by nonsteroidal anti-inflammatory drugs (NSAIDs), or related to Zollinger-Ellison syndrome. Helicobacter pylori-related ulcers can be treated by eradication of H pylori or by traditional therapies, including antisecretory drugs or sucralfate. Successful eradication of H pylori requires compliance with a multidrug regimen. Therefore, candidates should demonstrate substantial motivation. In general, the greater the degree of ulcer recurrence or resistance, the stronger the indication for H pylori eradication. Sucralfate is effective in healing H pylori-related duodenal ulcers, and H2 receptor antagonists heal H pylori-related duodenal and gastric ulcers. Omeprazole provides faster healing of H pylori-related ulcers, and is particularly useful in treating large gastric ulcers. Dyspepsia induced by NSAIDs and NSAID-related endoscopic erosions are managed by stopping NSAID use or reducing the dosage; administering NSAIDs with meals; and administering H2 receptor antagonists in full split-doses. NSAID-induced duodenal ulcers and small gastric ulcers can be healed with full split-doses of H2 receptor antagonists, even while the NSAID is continued. Large (> 5 mm) NSAID-induced gastric ulcers are most efficiently treated with omeprazole, particularly if the patient continues to take the NSAID.
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PMID:An etiologic approach to management of duodenal and gastric ulcers. 828 53

The proton pump inhibitors omeprazole and lansoprazole and the histamine H2 receptor antagonists ranitidine and nizatidine were investigated for their effects on gastric transmucosal potential difference (PD) in the rat, in comparison with the gastroprotective compound sucralfate. Omeprazole (1-3 mg kg-1, i.v.) and lansoprazole (1-3 mg kg-1, i.v.) did not modify basal PD, but significantly reduced (by approx. 50-60%) the drop in PD caused by intragastric administration of acetylsalicylic acid (ASA, 60 mg kg-1). Ranitidine (3-100 mg kg-1, i.v.) and nizatidine (10-30 mg kg-1, i.v.) behaved similarly to proton pump inhibitors, being ineffective on basal PD, while significantly reducing the effect of ASA. The antisecretory compounds did not change basal pH values. Sucralfate (0.5-1.5 g kg-1 intragastrically) caused a slight increase (approx. 20%) of basal PD and a dose-dependent reduction of ASA-induced fall in PD, with a maximum effect (65% reduction) comparable to that caused by the antisecretory agents. These results showed that ASA-induced disruption of the mucosal barrier can be reduced to the same extent by various antiulcer drugs, irrespective of their effects on gastric acid secretion.
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PMID:Effects of different antisecretory drugs on gastric potential difference in the rat: comparison with sucralfate. 999 Jun 56

Allophylus serratus is known to possess various therapeutic properties. We evaluated the anti-ulcerogenic property of crude ethanolic extract of Allophylus serratus (AS) in different ulcer models in Sprague-Dawley rats. The extract at 400 mg/kg body weight, once daily, orally has a significant effect in cold restraint (CRU, 2 h cold restraint stress), aspirin (ASA, 150 mg/kg body weight, orally), alcohol (AL, 1 ml/200 gm of absolute alcohol) and pyloric ligation (PL, 4h ligation) induced gastric ulcer models as it showed protection index of 71.28, 62.50, 90.84 and 64.29% protection, respectively whereas, standard drug omeprazole (OMZ, 10mg/kg body weight) has shown protection index of 85.70, 74.99 and 74.99 in CRU, ASA and PL model respectively. Sucralfate (SUC, 500 mg/kg body weight) as a standard drug in AL model has 93.20% protection. Furthermore, AS has significantly decreased the free acidity (72.41%), total acidity (47.97%) and peptic activity (24.59%), respectively as well as has significantly increased the mucus secretion (29.41%). Conclusively the ulcer protective effect of AS may be due to its anti-secretory along with cytoprotective mechanism.
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PMID:Allophylus serratus: a plant with potential anti-ulcerogenic activity. 1587 49