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 gastric duodenal mucosa normally is protected from the damaging effects of gastric acid and pepsin by ill-defined mechanisms. Ulcers may arise when there is an imbalance between the aggressive and defensive factors that renders the mucosa susceptible to damage. A variety of factors have been identified that may favor the development of peptic ulcers, but no single pathophysiologic defect applies in all ulcer patients. In duodenal ulcers, gastric acid hypersecretion is observed in as many as one third of patients; however, most patients with duodenal ulcers secrete normal amounts of gastric acid. Decreased mucosal bicarbonate secretion may be important in at least some duodenal ulcer patients. Use of NSAIDs may cause either gastric or duodenal ulcers, probably through the inhibition of mucosal prostaglandin synthesis and disruption of mucosal defenses. Finally, a recently identified bacterium, H. pylori, causes a chronic gastritis that is found in the overwhelming majority of patients with duodenal ulcers and non-NSAID-associated gastric ulcers. This bacterium may play a pivotal role in ulcer pathogenesis and, especially, in ulcer recurrences. A number of drugs of proved efficacy are available for the treatment of acute duodenal and gastric ulcers. The H2 receptor antagonists administered once daily remain the mainstay of ulcer therapy because of their efficacy, ease of use, and excellent safety profile. More thorough and long-lasting acid inhibition is afforded by the H+/K(+)-ATPase inhibitor omeprazole. This agent also promotes more rapid ulcer healing, but in most patients, this minor advantage may not justify the higher cost. It is not known whether more rapid healing will translate into lower ulcer complication rates. Until further data are available, this drug may be preferable in patients with large or complicated ulcers. In patients with refractory ulcers, omeprazole is clearly superior to other available agents. Agents that promote mucosal defense mechanisms are becoming increasingly popular in the treatment of duodenal ulcers but have undergone less testing than in gastric ulcers. Sucralfate 1 g four times daily is equivalent to H2 antagonists in the treatment of duodenal ulcers and, probably, gastric ulcers. Its requirement for multiple daily doses makes it somewhat less attractive at present to most patients. Low- to medium-dose Al-containing antacids are inexpensive and efficacious in duodenal ulcer therapy. They should remain as therapeutic options for the compliant patient in whom cost considerations are important. Colloidal bismuth subcitrate 120 mg four times a day is comparable to other agents in the acute treatment of duodenal ulcers and likely gastric ulcers.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Medical therapy of peptic ulcer disease. 134 60

Stress ulcer prophylaxis diminishes but does not eliminate the risk of severe bleeding from this complication. In 70-80% of the cases the source of bleeding is hemorrhagic gastritis. No controlled studies exist which have in particular investigated conservative therapy in patients with stress-induced hemorrhage. Even effective measures to suppress gastric acid secretion or to reduce splanchnic blood flow are ineffective in 10-40% of intensive care unit patients with stress-induced bleeding. In these cases total gastrectomy has so far often been the only therapeutic approach. We report our experience with a new approach in treating severe stress-induced hemorrhagic gastritis after ineffective primary treatment with H2-receptor antagonists, pirenzepine and somatostatin. Continuous gastric lavage with 5-10 l ice-cold Ringer's solution was used until complete cessation of bleeding, as evident from clear lavage. Repeated administration of 12 g sucralfate (60 ml) at 2-h intervals for 24 h through a gastric tube was used to prevent recurrence of bleeding and to promote healing. Sucralfate was reduced on the 2nd and 3rd day to 20 ml 2-hourly and later to 10 ml 4-hourly. In four patients this treatment was used as an ultima ratio when the patients were already scheduled for total gastrectomy. A total of 23 patients were treated during a 7-year period; all of them responded successfully, and no patient required surgery.
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PMID:Conservative treatment of stress ulcer bleeding: a new approach. 141 Dec 92

Twelve patients with active duodenal ulcer disease and Helicobacter pylori infection were treated with 1 g sucralfate q.d.s. for 1 month. Ulcers healed in 8 of the 12 patients without an alteration in the H. pylori-associated antral gastritis. Sucralfate produced a significant fall in basal acid output in all the patients, from a median of 4.8 (range 2.1-12.1) to 1.6 (0.4-8) mmol/h, P less than 0.01, whereas peak acid output was unchanged from 41 (21-59) before to 38 (24-55) mmol/h after treatment. Basal plasma gastrin concentrations and the meal-stimulated integrated gastrin response were not altered significantly by sucralfate: 8 (2-17) pmol/L and 732 (188-1045) pmol. min/L pre-treatment and 6 (2-17) pmol/L and 600 (140-1302) pmol. min/L post-treatment, respectively. The fall in basal acid output observed may contribute to prolonged duodenal ulcer remission after treatment with sucralfate.
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PMID:Sucralfate diminishes basal acid output without affecting gastrin, H. pylori or gastritis in duodenal ulcer patients. 160 44

Sucralfate plays an important role in peptic ulcer disease, reflux esophagitis, stress erosions and bleeding, and as adjunctive therapy in variceal sclerosis. In accordance with its pharmacologic characteristics, however, one may readily envisage disease states worth investigating, such as irradiation-induced mucosal damage of the esophagus. Especially the combination of external and intraluminal radiotherapy via the after-load technique may cause substantial and occasionally long-standing ulceration of the esophageal lining and discomfort. Several conditions of the stomach deserve further study. Increasingly common is gastric mucosal damage induced by aspirin or non-steroidal anti-inflammatory drugs. On the basis of its various pharmacologic principles sucralfate should theoretically offer protection against such lesions, and, in fact, there are human pharmacologic and clinical studies available supporting this idea. Another disease entity in which sucralfate should be studied in more depth is that of biliary alkaline reflux gastropathy as often seen after gastric surgery. Sucralfate should also be evaluated in those difficult clinical conditions known to be resistant to any therapeutic attempt with currently available drugs, such as erosive varioliform gastritis and hypertrophic gastropathy with heavy inflammation of the mucosa and giant coarsening of the gastric rugae. The results obtained with sucralfate in variceal sclerosis are indeed intriguing, even though the mechanism is not understood. It has been shown that sucralfate has some efficacy in patients with hemorrhagic gastritis. In many patients receiving chemotherapy, mucosal damage may occur both in the mouth and throughout the gastrointestinal tract, including the small bowel.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Future potential applicability of sucralfate in gastroenterology. 219 Mar 5

In a randomized trial involving 20 Italian centers, the effectiveness of 1 g sucralfate three times a day and 150 mg ranitidine twice a day in the treatment of chronic gastritis was assessed and compared. Five hundred outpatients with dyspeptic symptoms and endoscopic evidence of chronic nonerosive gastritis were randomly assigned to either treatment for a period of eight weeks. Endoscopic scores were determined at the beginning and at the end of the study. The severity of dyspeptic symptoms was assessed at Weeks 0, 2, 4, 6, and 8. Four hundred seventy-three patients completed the study. In 331 cases, biopsies were taken during endoscopy, and a histologic evaluation was also performed, according to Whitehead's criteria. Sucralfate was significantly more effective than ranitidine in inducing healing or improvement of both endoscopic (p less than 0.02) and histologic (p less than 0.001) features. At the end of the study, 77.6 percent of the patients in the sucralfate group and 79.4 percent in the ranitidine group were symptom free. Ranitidine was significantly more efficacious at releiving pain during the first four weeks of therapy. Mild side effects were reported by 4.9 percent of patients treated with sucralfate and by 3.6 percent of patients treated with ranitidine. Treatment was withdrawn in one patient treated with sucralfate because of nausea. In conclusion, sucralfate appears significantly superior to ranitidine in improving endoscopic and histologic aspects of chronic nonerosive gastritis. The symptomatic activity of the two drugs is similar, although more rapid relief is obtained with ranitidine.
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PMID:Comparison of sucralfate and ranitidine in the treatment of chronic nonerosive gastritis. A randomized, multicenter trial. 266 May 57

Sucralfate was synthesized to include a 75Se label, then compared with 111In-sucralfate and 99mTc-Human serum albumin (HSA)-sucralfate in vitro and in an animal ulcer model. The 75Se label was the only one of the three that was stable in both human gastric juice and simulated intestinal fluid in vitro. In rats with gastric ulcers, ulcer:nonulcer ratios of bound radioactivity averaged 15.4, 6.3, and 5.6 for 75Se, 111In, and 99mTc-HSA labels, respectively. Biodistribution studies of 75Se-sucralfate indicated that little is absorbed from the gastrointestinal tract, and the distribution is similar to that of 14C-sucralfate. Selective binding of 75Se sucralfate was successfully imaged in patients with esophagitis (esophageal mean T1/2 binding = 65 +/- 32 min), gastritis (gastric mean T 1/2 binding = 118 +/- 34 min), and gastric ulcers (ulcer mean T 1/2 binding = 135 +/- 59 min). Duodenal ulcers were not successfully imaged. Normal subjects showed no abnormal localization of sucralfate, and esophageal and gastric clearances were rapid.
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PMID:Selenium-75-labeled sucralfate: comparison with other radiolabels and initial clinical studies. 339 Mar 51

Gastritis has a wide spectre of definition modalities. Most previous studies have compared symptomatology with histologic gastritis with negative results. We believe that this may be due to inadequate definition criteria and emphasize this point by comparing gastroesophageal reflux with duodenogastric reflux. A prospective randomized trial has been conducted for half a year comparing Sucralfate with a placebo in patients with symptomatological and macroscopical gastritis. Although approximately one hundred patients met the endoscopic criteria, the vast majority could not be included due to well-defined interfering diseases, and thus the material is still too sparse to give any indication of the influence of Sucralfate on endoscopic gastritis, although the preliminary overall results seem promising.
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PMID:Sucralfate in gastritis. 347 71

Rats pretreated with dilute ethanol, dilute hydrochloric acid, or dilute sodium hydroxide had significantly less gastric mucosal damage when they were exposed 15 or 30 minutes later to strong irritants. The dilute agents, known as mild irritants, also caused an increase in the production of gastric mucosal prostaglandin E2 at the 15- and 30-minute dosing intervals. This suggests that the mild irritants are only effective in providing gastric mucosal protection when they increase gastric production of prostaglandin E2. Sucralfate treatment also caused an increase in gastric mucosal production of prostaglandin E2 at only the 15- and 30-minute dosing intervals. In contrast, pretreatment with sucralfate protected against the damaging effects of the strong irritants for at least 480 minutes. Therefore, prostaglandin E2 may play a role in sucralfate's protective effect at short dosing intervals, but at longer intervals, when prostaglandin E2 changes were not observed, sucralfate was still found to be very effective in reducing the severity of gastritis. This suggests that sucralfate acts, at least in part, through some other mechanism(s) besides increasing gastric mucosal prostaglandin E2 production.
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PMID:Effects of sucralfate or mild irritants on experimental gastritis and prostaglandin production. 347 60

The effects of sucralfate (6 g per day) and placebo on symptoms, endoscopic findings, and gastric mucosal histology were compared in 23 patients with symptoms of alkaline reflux gastritis who had undergone Billroth I, Billroth II, or vagotomy and pyloroplasty. Patients were randomly assigned to receive sucralfate (n = 11) or placebo (n = 12) for six weeks. Then all received six weeks of open sucralfate therapy before treatment codes were revealed. Twelve gastric biopsy specimens were obtained before patients began treatment and at six and 12 weeks. The two groups did not differ significantly with respect to symptom scores or endoscopic findings at baseline, after the double-blind phase, or after open sucralfate treatment. There were also no significant differences between the treatment groups with respect to epithelial cell scores and conventional gastritis scores. However, after the six-week, double-blind phase, the inflammatory cell score of the sucralfate-treated group was significantly lower (p less than 0.05) than that of the placebo-treated group (1.3 +/- 0.3 versus 1.9 +/- 0.4). After six weeks of open sucralfate treatment, patients who had initially received placebo had a significant reduction (1.4 +/- 0.3 versus 1.9 +/- 0.4) in their inflammatory cell score. Sucralfate lowered the inflammatory cell scores of patients with symptoms of alkaline reflux gastritis. This reduction, however, was not associated with an improvement in symptoms.
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PMID:Sucralfate therapy in patients with symptoms of alkaline reflux gastritis. A randomized, double-blind study. 383 73

The binding moiety of sucralfate to gastric mucosal sites, such as gastric ulcers and areas of gastritis, was studied in humans. The methods used to elucidate this binding were chemical assay of sucralfate, gastroscopic examination, and histological diagnosis in 39 patients with gastric ulcer and ten patients with gastritis. Sucralfate was observed in the gastric ulcer, and sucrose sulfate ester and aluminum were detected selectively in the lesions. In cases of chronic gastritis, there was no correlation between histological changes and the binding of the sucralfate, but the amount of adhesive mucus and the state of congestion were significantly correlated with the binding of sucralfate.
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PMID:Specific binding of sucralfate in gastric ulcer and gastritis. 668 56


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