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)

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

All nonsteroidal anti-inflammatory drugs (NSAIDs) used in the treatment of rheumatic diseases may cause gastric mucosal damage. Although the best-studied agent is aspirin, the mechanisms by which it damages the gastric mucosa are not fully understood. However, it is thought that the drug impairs mucosal defenses by penetrating the protective mucous and bicarbonate layers and damaging the epithelial lining cells. In turn, gastric acid is permitted to pour through the breached defenses. This "back-diffusion" of acid further injures cells and destroys capillaries and venules. This local damaging effect is pH dependent and is contributed to by the acid secretion of the stomach. Other mechanisms by which aspirin may induce or contribute to mucosal injury include inhibition of mucosal prostaglandin synthesis, reduction and alteration of mucus secretion, reduction of bicarbonate secretion, interference with cell turnover, as well as systemic effects such as platelet dysfunction. The mechanism by which nonaspirin NSAIDs cause gastrointestinal damage is uncertain. All are known to inhibit prostaglandin synthesis, which could contribute to their toxicity since prostaglandins found in the stomach both inhibit acid secretion and have mucosal defensive effects. Partial protections against aspirin-induced or other NSAID-induced gastric mucosal damage has been demonstrated, at least in some studies, by sucralfate, prostaglandins, omeprazole and histamine (H2)-receptor antagonists. Sucralfate appears to act primarily on local defensive mechanisms; its antisecretory effects are minimal. Prostaglandins exert a protective effect at both antisecretory and nonantisecretory (cytoprotective) doses, indicating that either or both mechanisms may be involved. The most recently studied agent, omeprazole, is the most potent of all acid inhibitors; it may also be cytoprotective, possibly as a result of its effects on sulfhydryl groups. Prostaglandins and omeprazole are not available in the United States and their potential side effects may limit their use in patients with chronic rheumatic diseases. Protection by H2-receptor antagonists is mostly related to reduction of acid secretion, though a cytoprotective effect may occur.
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PMID:Mechanisms of nonsteroidal anti-inflammatory drug-induced gastric damage. Actions of therapeutic agents. 289 63

Syrup of ipecac (SOI) is a commonly used emetic for toxic ingestions. A preliminary study was undertaken to quantify the efficacy of SOI-induced emesis. Three groups of adult subjects fasted overnight before ingestion of 1 mCi of Tc-99m human serum albumin-sucralfate. Sucralfate is minimally absorbed from the gastrointestinal tract and has a gastric clearance half-time of 90 minutes, approximately equal to that of solid foods. At 5, 30, and 60 minutes after ingestion of radiolabeled sucralfate (RSC), subjects were given a standard dose of 30 ml SOI and 240 ml of water. Gastrointestinal tract images were obtained both at the time of ingestion of RSC and 60 minutes after ingestion of SOI. Regions-of-interest were drawn and activity measured over the stomach and small bowel with correction for physical decay. Those subjects (N = 10) treated at 5 minutes after ingestion retained a mean value of 17% of the administered RSC by 60 minutes. The group (N = 5) treated at 30 minutes after ingestion retained a mean value of 41%, while those (N = 5) treated at 60 minutes retained a mean value of 56%. The results tend to confirm the efficacy of SOI-induced emesis when SOI is given promptly (i.e., 5 minutes) following ingestion, and generally support efforts to assure widespread immediate availability of SOI for toxic ingestions.
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PMID:Efficacy of syrup of ipecac-induced emesis for emptying gastric contents. 290 46

Both genetic and nongenetic factors predispose to ulcer diathesis. At the mucosal level ulcers result from an imbalance between aggressive factors and mucosal defense. Ulcer therapy reduces aggressive forces, bolsters defense, or both. Gastric acid, the major aggressive factor, may have its secretion inhibited or it may be partially neutralized by antacids. H2 receptor antagonists competitively block histamine occupancy of H2 receptors on parietal cells, thereby preventing stimulation of adenylate cyclase, cAMP rises, and activation of protein kinase and H+/K+ATPase. Prostaglandins inhibit acid secretion largely by preventing histamine-induced cAMP rises. Proton pump inhibitors bind H+/K+ATPase. Antimuscarinics inhibit acetylcholine receptors on the parietal cell, thereby blocking Ca2+ entry and subsequent activation of protein kinase and the proton pump. Mucosal defense is enhanced by certain prostaglandins, colloidal bismuth subcitrate and sucralfate. Prostaglandins stimulate secretion of bicarbonate and mucus, among other effects. Colloidal bismuth and sucralfate bind to proteins in the ulcer base and stimulate bicarbonate and mucus secretion, partially, in the case of sucralfate, by increasing endogenous prostanoid synthesis. Sucralfate also binds pepsin and bile acids. Colloidal bismuth temporarily eradicates mucosal colonization by Campylobacter pylori, another putative agent in ulcer diathesis.
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PMID:The pathophysiological and pharmacological basis of peptic ulcer therapy. 290 42

Mucosal lesions in the g.i. tract due to ASA and other nonsteroidal anti-inflammatory drugs are well-known in clinical practice. Though the gastroduodenal mucosa is the area most commonly investigated, several recent reports focus on lesions in the small and large intestine as well. Despite considerable efforts in the field, none of the new substances developed in the past few years have proven convincingly superior to existing drugs. Instead, other approaches are being evaluated: Bypassing of the gastroduodenal mucosa through enteric coating and slow release formulations have been suggested, but the possibility of transferring the deleterious effects to distal parts of the gastrointestinal tract by such formulation modifications calls for extensive evaluation of this area, before these formulations can be applauded as advantageous in this group of patients. Co-administration of protective substances has also been advocated, and, despite somewhat contradictory results, protection has been reported by H2-antagonists alone or in combination with antacids, as well as by cytoprotective agents like Sucralfate, and prostaglandin analogues.
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PMID:Management of NSAID-induced gastrointestinal lesions. 290 80

Sucralfate has been reported to reduce serum phosphate concentration in patients with chronic renal failure. To evaluate whether sucralfate could be used to treat hyperphosphatemia secondary to chronic renal failure and whether this treatment resulted in a reduced exposure to aluminum, an open-label crossover study was designed to determine the efficacy, relative potency, safety, and cost of sucralfate v aluminum hydroxide. Of the 21 hemodialysis patients completing both phases of the crossover study, serum phosphate could be maintained below 4.5 mg/dL (1.45 mmol/L) in 16 with sucralfate and in 14 with aluminum hydroxide. The 16 patients controlled on sucralfate consumed 1,694 +/- 190 mg/d of aluminum to maintain a serum phosphate concentration of 3.91 +/- 0.17 mg/dL (1.27 +/- 0.05 mmol/L) compared with the 14 patients controlled on aluminum hydroxide with an aluminum intake of 2,678 +/- 294 mg/d (P less than 0.025) and a serum phosphate concentration of 3.94 +/- 0.13 mg/dL (1.27 +/- 0.04 mmol/L). Thus sucralfate was an effective, albeit expensive, alternative to aluminum hydroxide for the treatment of hyperphosphatemia associated with chronic renal failure. Although the difference in aluminum intake was significant, use of sucralfate did not result in lower serum aluminum concentrations.
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PMID:Phosphate-binding effects of sucralfate in patients with chronic renal failure. 291

The efficacy of orally administered sucralfate suspension in preventing and treating chemotherapy-induced mucositis was evaluated in a double-blind trial. Forty-eight children and adolescents with newly diagnosed acute nonlymphocytic leukemia were randomized to receive suspensions of either sucralfate or placebo orally every 6 hours during the first 10 weeks of intensive remission-induction chemotherapy. Patients given sucralfate suspension were less likely than subjects receiving placebo to acquire colonization with potentially pathogenic microorganisms: 14 (58%) of 24 versus 22 (92%) of 24, respectively (p = 0.008). However, no effect on preexisting colonization was noted. Subjective reporting of discomfort, objective scoring of the severity of mucositis, and the maximal percent of body weight lost during therapy were similar; 58% of patients receiving sucralfate reported no oral pain compared with 25% receiving placebo (p = 0.06). Ten episodes of gastrointestinal bleeding, 25 documented infections, and 886 days with fever were also equally distributed between sucralfate and placebo groups. We conclude that sucralfate suspension is of limited, if any efficacy, in the prevention and treatment of chemotherapy-induced mucositis. Sucralfate administration can, however, reduce acquisition of alimentary colonization with potential pathogens, perhaps by interfering with adherence to mucosal membranes.
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PMID:Efficacy of oral sucralfate suspension in prevention and treatment of chemotherapy-induced mucositis. 305 5

Misoprostol, a PGE1 derivative that inhibits gastric acid secretion in rats, was compared with cimetidine and sucralfate in several rat experimental ulcer models. Gastric lesions were produced by aspirin, indomethacin, stress, sodium taurocholate, and ethanol. In all tests, misoprostol (50, 100, and 200 micrograms/kg) and cimetidine and sucralfate (50, 100, and 200 mg/kg) were administered intragastrically. Misoprostol protected against gastric lesions in all five experimental ulcer models at lower than gastric antisecretory doses. Cimetidine protected in the indomethacin, aspirin, and stress models, but only at gastric antisecretory doses, and did not protect against lesion formation in the ethanol and taurocholate models. Sucralfate, over the dose range tested, was not consistently protective in any of the five experimental ulcer models. It is concluded that misoprostol provides gastric mucosal protection against a wide variety of noxious agents by means of a unique mechanism and that reduction of gastric acid secretion is not required, as it is with cimetidine, for the protective effect.
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PMID:Comparative mucosal protective properties of misoprostol, cimetidine, and sucralfate. 308 Feb 94

The protective effect of sucralfate against gastric and intestinal mucosal damage was studied in rats. Sucralfate (125 mg) significantly reduced gastric mucosal lesion formation induced by s.c. administration of indomethacin (30 mg/kg) or intragastric administration of aspirin (100 mg/kg), HCl (0.6 N), NaOH (0.2 N) or sodium taurocholate (30 mM). Furthermore, when given in three doses of 125 mg each, sucralfate significantly decreased the development of small intestinal lesions induced by indomethacin in the re-fed rat. Gastric mucosal cyclooxygenase activity in sucralfate-treated rats expressed as prostaglandin E2 formation--388 +/- 140 (ng/g wet weight; mean +/- SE)--was significantly higher (P less than 0.01) than its activity in the control--264 +/- 62 (ng/g wet weight). Sucralfate also slightly, but significantly, decreased indomethacin-induced gastric mucosal cyclooxygenase inhibition. Intestinal mucosal cyclooxygenase activity was not affected by sucralfate. The results suggest that gastric and intestinal mucosal damage induced by various ulcerogens is significantly reduced by sucralfate. Sucralfate-induced stimulation of endogenous gastric mucosal prostanoid formation may in part explain its effective protective properties.
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PMID:Sucralfate protection against gastrointestinal damage: possible role of prostanoids. 309

Stress ulcers are a frequently encountered problem in critically ill medical patients. Gastric acid and decreased gastric mucosal blood flow appear to be important in the pathogenesis of these lesions. Occult bleeding from stress ulcers is common, although significant bleeding occurs in less than 20% of patients. The mortality of bleeding is dependent on the severity of the underlying diseases. A number of processes have been suggested as risk factors; however, prolonged mechanical ventilation, a coagulopathy, and the presence of more than one risk factor place the patient at greatest risk. Titration of the gastric pH to greater than four with either antacids or H2-receptor antagonists provides effective prophylaxis. The continuous infusion of the H2-receptor antagonists is also efficacious. Sucralfate appears to be another useful alternative with several potential advantages. Prophylactic therapy decreases the incidence of stress ulcer-related bleeding, although it does little to improve the survival of the critically ill patient.
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PMID:Stress ulcer prophylaxis in medical patients: who, what, and how much? 314 49


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