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)

Peptic esophagitis is a common complication of gastroesophageal reflux. Therapeutic measures aimed at reinforcing the anti-gastroesophageal reflux barrier, reducing acid secretion, or increasing the defense mechanisms of the esophageal mucosa are used to treat this form of esophagitis. The purpose of this study was to determine the efficacy of sucralfate in the treatment of peptic esophagitis in children. We studied 75 patients diagnosed endoscopically as suffering from esophagitis. The age of the patients ranged from three months to 13 years. Gastroesophageal reflux was diagnosed by isotopic investigation and/or radiologically. None of the patients had kidney disease or had received anti-inflammatory drugs, sucralfate, or cimetidine during the preceding two weeks. The patients were divided into three groups of 25. Patients were homogeneous in age, sex, nutritional status, symptoms, and grade of esophagitis. All patients in each group were treated with cimetidine, sucralfate tablets, or sucralfate suspension. No other dietary or postural measures were prescribed. Clinical examinations were carried out on Days 14, 28, 42, and 56, with an endoscopic examination on Day 28. Endoscopy was repeated on Day 56 if the course was unsatisfactory. Statistical examination of the data showed that there were no differences between the three groups. Sucralfate is a useful drug for the treatment of peptic esophagitis in children.
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PMID:Sucralfate versus cimetidine in the treatment of reflux esophagitis in children. 273 38

Gastric emptying studies were performed on nine healthy volunteers and ten duodenal ulcer (DU) patients utilizing a dual radionuclide technique to assess simultaneously emptying rates of liquid (111In labeled water) and solid (99mTc sulfur colloid labeled chicken liver) components of a meal. One gram of sucralfate was compared to placebo in separate days in a randomized double-blind crossover fashion. Subjects ingested the radiolabeled test meal 1 h after receiving medication, and gastric emptying was monitored for 3 h using a gamma camera interfaced with a computer. We found that DU patients had significantly faster gastric emptying of solids (P less than 0.05) compared to normals on the placebo days, while liquid emptying rates were similar. Sucralfate, in the DU patients, significantly (P less than 0.05) slowed gastric emptying of water from 20 to 40 min and emptying of the solid component from 100-160 min after the meal compared to placebo. In normal subjects, gastric emptying of liquids and solids was not significantly affected by sucralfate. We conclude that slowing of gastric emptying, possibly mediated through aluminum ions, occurs in DU patients on sucralfate. This may be one mechanism by which sucralfate enhances healing and decreases recurrence of duodenal ulcer.
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PMID:Sucralfate delays gastric emptying of liquids and solids in duodenal ulcer patients. 277 80

Sucralfate exhibits gastroprotective properties in laboratory animals and enhances the healing of chronic gastroduodenal ulcers, but the mechanisms of these actions have not been entirely elucidated. The present study was designed to determine whether or not epidermal growth factor (EGF), which also has gastroprotective and ulcer-healing properties, contributes to the action of sucralfate in rat stomach. It was confirmed that sucralfate, like 16,16-dimethyl prostaglandin E2, protects the gastric mucosa against ethanol damage and increases mucosal generation of prostaglandins. Removal of the endogenous source of EGF (sialoadenectomy) did not abolish the protective and prostaglandin-stimulating effects of sucralfate. Exogenous EGF and 16,16-dimethyl prostaglandin E2 were also protective in rats with intact and removed salivary glands. Sucralfate, like EGF, enhanced the healing of chronic gastric and duodenal ulcerations induced by serosal application of acetic acid. Sucralfate was found to bind EGF in a pH-dependent manner and to accumulate it in ulcer areas. Thus, the peptide is available locally in high concentrations to accelerate tissue repair and the healing process in ulcerated mucosa. The ulcer-healing effects of sucralfate were reduced with sialoadenectomy and partially restored with oral administration of EGF. It was concluded that EGF is not essential for the gastroprotection induced by sucralfate, but seems to play an important role in the ulcer-healing action of this drug.
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PMID:Epidermal growth factor in the gastroprotective and ulcer-healing actions of sucralfate in rats. 278 72

The effect of Campylobacter pylori infection and sucralfate treatment on the ion-exchange property of human gastric mucus from 17 human postmortem stomachs was investigated in an in vitro chamber. Of the 10 stomachs not infected with C. pylori mucus from 4 stomachs had a 'normal' Na+/H+ exchange capacity, whereas 6 were without a Na+/H+ exchange capacity. The Na+/H+ exchange capacity of the seven stomachs infected with C. pylori was half that of the four 'normal' uninfected stomachs. Sucralfate significantly improved the Na+/H+ exchange capacity of mucus from C. pylori-infected stomachs and from the uninfected stomachs without Na+/H+ exchange. This study shows that impairment of the Na+/H+ exchange capacity of gastric mucus is associated with C. pylori infection and that sucralfate improves the Na+/H+ exchange capacity of gastric mucus.
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PMID:Na+/H+ ion-exchange property of postmortem human gastric mucus. The effects of Campylobacter pylori infection and sucralfate. 279 81

Standard oesophageal scintigraphic techniques using 99mTc-colloids rarely identify oesophageal mucosal damage. Sucralfate can be labelled with 99mTc for the detection of oesophageal mucosal ulceration. This method uses two separate supine swallows of 10 MBq 99mTc-colloid in 10 ml, followed by a single supine swallow of 30 MBq 99mTc-sucralfate. The data are processed to give time-activity curves, mean transit times and condensed dynamic images. When oesophageal ulceration is detected, the time-activity curves using sucralfate show residual activity in the oesophagus after the transit time indicated by the colloid swallow. The condensed dynamic image shows a persistence of activity at the level of the ulceration. Erect sucralfate images taken immediately after the dynamic sequence show no oesophageal localisation. The results from a study of 62 patients have shown excellent correlation between the dynamic 99mTc-sucralfate images and endoscopy findings. Sequential sucralfate studies for healing also correlate well. The use of labelled sucralfate to detect oesophageal ulceration could modify the indications for endoscopy in gastrooesophageal reflux disease.
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PMID:Dynamic radionuclide imaging with 99mTc-sucralfate in the detection of oesophageal ulceration. 280 94

Fifty patients in whom endoscopy revealed peptic esophagitis were included in a double-blind study in which either sucralfate (1 g four times a day) or an alginate/antacid compound (5 g four times a day) were randomly assigned. After six weeks of treatment, efficacy and clinical safety were evaluated in 23 patients in the sucralfate group and 22 patients in the alginate/antacid group. No significant difference between the two treatments was detected with regard to efficacy, evaluated on the basis of clinical and endoscopic criteria. Clinical safety was also good in both groups. Sucralfate was, therefore, found to be as effective and as well tolerated as the alginate/antacid compound in the treatment of peptic esophagitis.
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PMID:Sucralfate versus alginate/antacid in the treatment of peptic esophagitis. 282 8

The first part of the study consisted of 110 rats in 11 groups with ten rats in each. Nine of the groups were fed nutrient solutions of different compositions, antacid and sucralfate through orogastric tube during induction of stress ulcer by restraint and a cold ambient temperature. One group served as a control group and received no feeding and the 11th group was given cimetidine intraperitoneally. The extensiveness of the stress effect was estimated in each group by the number of rats with ulcer as percentage, the mean number of ulcers in each rat, the mean distribution of ulcers of different sizes, the mean total of mucosal damage in each rat and the contribution of ulcers of a different size to the total mucosal damage. The results showed that cimetidine is an effective protector against stress ulcer. Guar gum, Intralipid (fat emulsion), egg protein and 30 per cent glucose are slightly weaker protectors than cimetidine but much stronger than 10 per cent glucose wheat flour and distilled water. Sucralfate increased the susceptibility to stress ulcer. The second part of the study consisted of 86 rats. It showed, that guar gum increased the healing rate of stress ulcers. During a 30 hour treatment period after four hours of stress, the rats fed guar gum (n = 30) showed a lower (p less than 0.001) number of ulcers than the control rats fed normal rat food (n = 26) or immediately after the four hours of stress (n = 30). The mechanisms suggested for ulcer prevention and increased ulcer healing rate found herein may be due to reduced acidity, increased local mucosal supply of energy and mechanical protection.
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PMID:The protective effect of nutrients against stress induced gastric ulcers in the rat. 282 67

Until 1950 the clinical treatment of peptic ulcer disease relied on dieting and antacids. However, recent controlled studies suggest that the natural course of peptic ulcer disease is not affected by diet. Antacids are primarily used to relieve distress, although high- and low-dose antacid regimens have been reported to promote duodenal ulcer healing. Initial favorable reports following the introduction of synthetic anticholinergic drugs have not been confirmed. Pirenzepine is an anticholinergic compound with a specific action on the muscarinic receptors of the parietal cells. Although pirenzepine appears effective in peptic ulcer, the results obtained in different centers have not been uniform. Sucralfate and tripotassium dicitrato bismuthate both act locally by coating the ulcer crater, the latter agent also liberating prostaglandins. Most prospective studies suggest that both drugs are effective when compared with placebo. Carbenoxolone heals 70% of gastric ulcers but is less effective against duodenal ulcers, and has a high incidence of side-effects. Treatment of peptic ulcer in the 1980s has been dominated by the advent of the H2-blockers, cimetidine and ranitidine. Peptic ulcer healing rates are similar with both drugs, and the main problem is how often and how much should be given in order to provide acceptable healing and to prevent ulcer recurrence. Other H2-blockers are being tested and they may be more effective either by healing more ulcers or healing them earlier. The clinical treatment of peptic ulcers will in future be advanced by the addition of two new classes of drugs, the prostaglandins and the benzimidazole derivatives, which are currently being investigated and appear extremely promising.
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PMID:Anti-ulcer therapy. Past to present. 286 91

Stress-related mucosal damage (SRMD) of the upper gastrointestinal tract is being increasingly recognized in critically ill patients. Its precise pathogenesis is unknown. Acid is a prerequisite for the development of mucosal injury. However, mucosal defense factors that maintain the integrity of the gastric mucosal barrier are equally important. Therapy is directed toward reducing the intraluminal acid concentration. Since histamine H2-receptor antagonists became available in 1977, they have been used for the prevention and treatment of SRMD. They offer the potential for use as an effective parenteral as well as oral agent that could obviate the need for frequent antacid administration and eliminate some of the troublesome side effects that accompany an intensive antacid regimen. Although the beneficial effects of H2 blockers are probably related to their ability to inhibit acid secretion, recent evidence suggests that they may also act by mechanisms independent of their antisecretory effect. Numerous controlled studies have confirmed that cimetidine, being superior to placebo and equivalent to antacids, is effective therapy for SRMD. Sucralfate, a basic aluminum salt of sucrose octasulfate, has been shown to protect animal and human gastric mucosa from a variety of injurious agents. However, few clinical trials have evaluated the efficacy of sucralfate in SRMD. Exogenous prostaglandins also have been shown to protect gastric mucosa from a variety of insults. Although exogenous prostaglandins may work by augmenting mucosal defense mechanisms, most clinical studies have used antisecretory doses of prostaglandin drugs, making it difficult to discount the antisecretory component as being responsible for efficacy.
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PMID:Stress-related mucosal damage. 287 27

Critically ill patients are prone to stress-induced ulcerations in the upper gastrointestinal tract, which might lead to life-threatening bleeding. Therefore, an effective stress ulcer prophylaxis is absolutely indicated and H2-blocking agents, anticholinergics, antacids, sucralfate, enteral nutrition and prostaglandin E analoges are recommended. H2-blocking agents seem to provide effective prophylaxis, but severe side effects seem to limit their application. Most of all, as they are less effective as antacids and as they cause considerable costs. Additionally H2-blocking agents elevate gastric pH, thereby favouring microbic colonisation of gastric juice. Microorganism from gastric juice may reach the tracheobronchial system and lead to nosocomial pneumonias. The contaminated gastric juice may also be considered as endogenous source for sepsis and entero-colitis. The anticholinergic agent pirenzepine does not increase gastric pH and seems to be effective in neurological and neurosurgical intensive care patients. Antacids are effective in stress ulcer bleeding prophylaxis, but favour bacterial overgrowth, are badly tolerated by patients and cause a high amount of nursing time. Sucralfate seems to be as effective as antacids, is better tolerated and does not elevate gastric pH. The remaining acidity of gastric juice blocks bacterial contamination. After all, the smallest costs of effective stress ulcer prophylaxis, makes sucralfate to the medicament of first choice. However, in severely ill patients, a combined stress ulcer prophylaxis with two or more agents seems to be necessary.
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PMID:[Prevention of stress ulcer in intensive care patients]. 288 1


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