Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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 complete purification of the first angiogenic molecule, basic fibroblast growth factor (bFGF), was carried out in the authors' laboratory in 1983. Application of this peptide to chronic wounds enhances angiogenesis and accelerates wound healing. The authors showed that an acid-stable form of bFGF (i.e., bFGF-CS23) could be administered orally to rats with duodenal ulcers. The peptide promoted a ninefold increase of angiogenesis in the ulcer bed and accelerated ulcer healing more potently than cimetidine. Basic fibroblast growth factor did not reduce gastric acid. The authors now show that bFGF exists as a naturally occurring peptide in rat and human gastric and duodenal mucosa. This endogenous bFGF is present also in the bed of chronic ulcers in rats. Sucralfate binds bFGF and protects it from acid degradation. The sucralfate is angiogenic, based on its affinity for bFGF. When sucralfate is administered orally to rats, it significantly elevates the level of bFGF in the ulcer bed. Cimetidine, by its capacity to reduce gastric acid, also elevates bFGF in the ulcer bed. A hypothetical model is proposed in which prevention of ulcer formation or accelerated healing of ulcers by conventional therapies may be FGF dependent. Acid-stable bFGF-CS23 may be considered as a form of replacement therapy in the treatment of duodenal ulcers.
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PMID:Duodenal ulcer. Discovery of a new mechanism and development of angiogenic therapy that accelerates healing. 171 45

Conventional stress bleeding prophylaxis with antacids or histamine (H2)-antagonists, as well as the newer mucosa-protective drugs pirenzepine and sucralfate, are satisfying most of the clinicians with regard to efficacy of stress bleeding prevention. Therefore, potential side effects are attaining crucial importance with regard to the drugs to be used. Pharmacologic blockade of cardiac H2-receptors increases the risk of bradycardia and negative inotropic effects as well as coronary vasoconstriction at least in the presence of elevated plasma histamine levels. Intracardiac injection of pirenzepine can lead to temporary tachycardia. Elderly patients have been shown to be at an increased risk of side effects to the central nervous system when treated with H2-antagonists. These drugs can also induce toxic effects in the liver. Cimetidine leads to interactions with a number of drugs used in the intensive care unit. In patients with pre-existing pulmonary diseases, H2-antagonists have been demonstrated to increase pulmonary bronchoconstriction. Alkalinization of the gastric juice is associated with a significant increase in colonization of gram-negative bacteria in the stomach. In intubated patients, aspiration of stomach contents occurs in 30 to 40 percent of the patients. A number of studies have shown a direct correlation between alkalinization of the gastric juice and pulmonary infections. Sucralfate and to a lesser degree pirenzepine can reduce the risk of pulmonary infections. Sucralfate also exerts a bactericidal effect. Recent investigations support the hypothesis that alkalinization of the stomach also increases the risk of systemic infections. This may be the main reason for the observation that at least in ventilated patients sucralfate, unlike H2-antagonists or antacids, leads to a significant reduction of the mortality rate compared with conventional stress bleeding prophylaxis.
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PMID:Side effects of stress bleeding prophylaxis. 256 72

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

Medical ulcer therapy focuses on enhancing mucosal defence mechanisms or reducing intraluminal acidity. In this Swedish multicenter, randomized double-blind study these two principles were compared in the treatment of acute duodenal ulcerations. Sucralfate (Andapsin 1g X 4) or cimetidine (Tagamet 400mg X 2), together with antacid tablets (Novalucol), were supplied to patients with acute ulcerations in the pyloric ring or duodenal bulb. Endoscopy was performed at inclusion, after four weeks and in some patients also after eight weeks. Besides healing rate, symptoms and antacid intake, smoking and side effects were recorded on a special protocol. 371 patients from 15 centers completed the trial. At inclusion the patient groups did not differ in any essential aspect. At four weeks 71% of 177 patients on sucralfate and 77% of 194 on cimetidine were healed. The corresponding figures for eight weeks were 86% (suc) and 92% (cim). The difference is not significant, the 95% confidence interval for the difference in ulcer healing efficacy of sucralfate compared with cimetidine at eight weeks was -12% to +5%. Antacid intake and symptoms decreased rapidly and equally in both groups. Side effects related to the treatments were uncommon. It is concluded that sucralfate and cimetidine, representing two different principles in medical ulcer treatment, are both very effective and compare well in the short term treatment of acute duodenal ulcer.
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PMID:Treatment of acute duodenal ulcer--a Swedish multicenter study. 330 93

The effects of OGT, SST, AS and DST on ethanol- and aspirin-induced gastric hemorrhagic lesions in rats were studied in comparison with those of sucralfate, 16,16-dimethyl-prostaglandin E2 (DMPGE2) and cimetidine. 1) OGT given orally at doses of 25-250 mg/kg protected gastric mucosa from injury induced by ethanol or aspirin. 2) SST prevented the appearance of aspirin-induced lesions at doses more than 25 mg/kg, and ethanol-induced lesions at 250 and 500 mg/kg. 3) AS and DST inhibited aspirin-induced lesions at more than 250 mg/kg and inhibited ethanol-induced lesions at 500 mg/kg. 4) Sucralfate (500 mg/kg) significantly prevented ethanol- and aspirin-induced lesions. DMPGE2 significantly inhibited ethanol-induced lesions at doses more than 0.1 micrograms/kg, and it inhibited aspirin-induced lesions dose-dependently at doses ranging from 0.1 to 5 micrograms/kg. Cimetidine significantly inhibited aspirin-induced lesions at doses of 10-250 mg/kg and inhibited ethanol-induced lesions at doses of 100 and 250 mg/kg. These results suggest that OGT, SST, AS and DST have a prophylactic effect on ulcerogenics, and the potency of OGT may be superior to those of SST, AS and DST.
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PMID:[Pharmacological studies on the effects of some traditional Chinese medicines on gastric functions. (3) The effects of oren-gedoku-to (OGT), san'o-syasin-to (SST), antyu-san (AS) and dai-saiko-to (DST) on ethanol- and aspirin-induced gastric lesions in rats]. 341 Mar 79

Ulcer relapses after short-term treatment of duodenal, prepyloric and gastric ulcers with Cimetidine 400 mg b.d. or Sucralfate 1 g q.i.d. were studied in 270 patients over one year. Endoscopic examinations were carried out 2-4 and 9-11 months after ulcer healing or when symptoms occurred. Ulcer relapses were found in 59% of the Cimetidine-treated patients and 51% of those treated with Sucralfate, and a further 21% and 16% respectively had endoscopically verified erosive gastroduodenitis. The cumulative recurrence rate in smokers was 82% and that in non-smokers 51% (p less than 0.001). Relapses among the Cimetidine patients occurred more often in those who smoked or had irregular working hours. The onset of the relapse was not related ulcer healing time. The ulcer relapses appeared in the same region as the initial ulcer in 88% of cases and exactly at the original site in 33%. These results suggest that cytoprotection by Sucralfate did not result in fewer or later relapses than acid reduction by Cimetidine. Cigarette smoking obviously increases the risk of relapse in patients with healed peptic ulcers.
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PMID:Ulcer recurrences following initial ulcer healing with sucralfate or cimetidine. 347 70

In order to study whether sucralfate or cimetidine may protect human gastric mucosa against alcohol injury, 28 healthy volunteers were pretreated with either: (1) placebo 1 g; (2) cimetidine (Tagamet) 300 mg; or (3) sucralfate (Carafate) 1 g. One hour later, 100 ml of 40 percent ethanol was sprayed directly on the gastric mucosa of the greater curvature during an endoscopic examination. Gastric mucosal changes were assessed by endoscopic appearance (according to grading scale) and by histology. In placebo-pretreated subjects, alcohol produced prominent mucosal damage (endoscopic score, 3.9 +/- 0.3, histologic score, 4.0 +/- 1.1 at 30 minutes). Cimetidine alkalinized gastric pH but did not prevent alcohol-induced damage (endoscopic score, 4.0 +/- 0.6; histologic score, 3.8 +/- 1.1, at 30 minutes). Sucralfate reduced endoscopic and histologic features of alcohol injury (endoscopic score, 1.8 +/- 0.6; histologic score, 1.8 +/- 1.1, at 30 minutes) without affecting gastric luminal pH. Reduction of alcohol-induced injury of the human gastric mucosa by sucralfate but not cimetidine demonstrates that effective protection of the gastric mucosa can be achieved without neutralization or inhibition of gastric acid secretion and points out another clinical application for sucralfate.
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PMID:Efficacy of sucralfate and cimetidine in protection of the human gastric mucosa against alcohol injury. 366 9

Cimetidine absorption after a single 300 mg oral dose was evaluated in six normal subjects in the absence or presence of sucralfate. Sucralfate was ingested four times a day for 2 days prior to and for two additional doses on the day of cimetidine ingestion. Sucralfate coadministration had no statistically significant influence on the rate or extent of cimetidine absorption.
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PMID:Cimetidine absorption in humans during sucralfate coadministration. 375 52

In this prospective study for pharmacotherapy of non varicial upper gastrointestinal haemorrhage eight therapy groups were examined. The efficacy of the most important drugs for ulcus disease was considered. The drugs were used alone and in combination. The results indicated no favourable effect of one preparation (Cimetidine, Pirenzepine, Ranitidine). Significant benefit for the long time healing rate was noted among the combination therapies, especially with Sucralfate, which was not used alone.
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PMID:[Conservative therapy of upper gastrointestinal hemorrhage (prospective, randomized, controlled)]. 387 31

In the United States, the drugs most commonly used to treat peptic ulcer disease are antacids and the H2-receptor antagonists cimetidine and ranitidine. Other available agents include anticholinergics and the coating agent sucralfate. Investigational drugs such as colloidal bismuth, carbenoxolone, prostaglandins, the tricyclic compound pirenzepine, and substituted benzimidazoles are not available for use in the United States. Most of the commercially available and investigational compounds have similar efficacy; therefore the optimal drug may be the one associated with the fewest adverse effects and the most convenient dosing regimen. Cimetidine causes a small number of adverse effects, including neuropsychiatric disorders, gynecomastia, impotence, loss of libido, elevation of serum creatinine and serum transaminases concentrations, and drug interactions. Some of these reactions have been of clinical significance. Presently, there are rare reports of gynecomastia, bradycardia, inhibition of acetylcholinesterase, headache, lethargy, diarrhea, and rash in patients receiving ranitidine. Antacids can produce either diarrhea or constipation and have been associated with low serum phosphorus concentrations, and metabolic alkalosis. Anticholinergics, especially in elderly or debilitated patients, can cause central nervous system disorders, intestinal atony, or urinary retention. Sucralfate may cause constipation, diarrhea, nausea, and headache. The investigational agents have their own side effect profiles. The adverse effects of anticholinergics make them unattractive therapeutic choices, and antacids and sucralfate have inconvenient dosing requirements compared with some equally efficacious alternatives. In addition, clinical experience with sucralfate in the United States is limited. The safety record of cimetidine is admirable. As clinical experience with ranitidine increases, currently unrecognized adverse effects may be reported. However, based on current data, ranitidine is as effective as cimetidine and is associated with a lower incidence of side effects.
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PMID:Problems associated with medical treatment of peptic ulcer disease. 609 62


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