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 antiulcerogenic and antipeptic activities of sucralfate (Ulcerlmin), a basic aluminum sucrose sulfate complex, were investigated. In rats, sucralfate inhibited the formation of ulcers induced by pyloric ligation, indometacin and cysteamine. In doses antagonizing forestomach ulcer formation, sucralfate increased the pH of the gastric juice in a dose-related manner. In vitro, at pH 1.9, sucralfate inhibited rat, dog and hog pepsin in a concentration-related manner and also the peptic activity in human gastric juice. Sucralfate may act as an inhibitor of pepsin by precipitating the enzyme or by binding with it reversibly. The antipeptic activity appears to be directly related to the amount of sucralfate in suspension rather than that in solution. In the gastrointestinal tract, the basic nature of sucralfate may enhance the antipeptic activity of the sucralfate molecule. In rats, sucralfate decreases the rate of gastric emptying.
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PMID:Sucralfate: antipeptic, antiulcer activities and antagonism of gastric emptying. 38 45

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

Topically active agents (i.e., colloidal bismuth subcitrate and sucralfate) have proved to be effective in promoting the healing of both gastric and duodenal ulcers and in relieving ulcer symptoms. Sucralfate alone has also been shown to maintain peptic ulcers in remission when taken continuously for a long period of time, whereas successful short-term therapy with bismuth subcitrate is associated with a more prolonged remission of duodenal ulcer disease when compared to H2 blockers. The antiulcer efficacy of these agents is partially counteracted by the need for multiple daily administrations, which requires greater patient compliance than with H2 antagonists. A specific subgroup of patients who might particularly benefit from these drugs are those with duodenal ulcer resistant to H2 blockers, whereas chronic nonsteroidal antiinflammatory drug users with peptic ulcer respond to therapy with site-protective agents as well as to antisecretory drugs.
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PMID:Topically active drugs in the treatment of peptic ulcers. Focus on colloidal bismuth subcitrate and sucralfate. 134 53

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

Tonsillectomy results in severe throat pain, ear pain, and trismus until the exposed and inflamed muscle becomes covered with regenerated mucosa. Sucralfate binds with the fibrinous exudate of duodenal ulcers, forming a protective barrier that promotes healing. If a similar buffer could be created in the tonsillar bed, morbidity may be diminished. A double-blind, randomized study was completed in 34 adult patients to determine whether sucralfate, given four times daily for 10 days as a swish and swallow, would significantly reduce postoperative pain and promote healing and recovery. Sucralfate significantly lowered postoperative throat pain, otalgia, and trismus. Sucralfate is a safe and well-tolerated topical agent that offers significant pain reduction and may promote healing in tonsillectomy patients.
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PMID:Sucralfate in alleviating post-tonsillectomy pain. 140 84

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

Sucralfate has a complex effect on the luminal and mucosal environment of the stomach and duodenum. Some of the actions are important in ulcer healing whilst others are important in preventing subsequent ulcer relapse. Although sucralfate has little direct effect on acid secretion, there is evidence that after ulcer healing with this drug, parietal cell responsiveness is reduced. This may in part be mediated by increased somatostatin release from gastric D cells and may be important in reducing ulcer relapse. Sucralfate has been shown to increase mucosal resistance to damaging agents, such as ethanol and aspirin. Studies have shown that this protective action may be related to the drugs effect on various protective zones such as the 'mucous-bicarbonate' barrier, mucosal hydrophobicity, epithelial cell function and morphology, and mucosal blood flow. These complex actions of sucralfate are in part related to direct interaction between the drug or its components and gastroduodenal tissues, and in part related to effects on various mediators of tissue injury and repair.
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PMID:Prevention of peptic ulcer relapse by sucralfate: mechanisms of action. 141 Dec 95

We have studied the effect of the aluminum complex of sucrose sulphate (Sucralfate suspension) and the sodium salt of sucrose sulphate (sodium sucrose sulphate solution) on patients with keratoconjunctivitis sicca. Eyes treated with either of these two drugs showed a decrease in painfulness and blurring of vision. On examination the surface area of the corneal lesions, stained with fluorescein, diminished during treatment. As for the difference in effect between the two eyedrops, the solution was better tolerated.
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PMID:Sucralfate and sodium sucrose sulphate in the treatment of superficial corneal disease in keratoconjunctivitis sicca. 141 98

In the course of a prospective selective digestive decontamination (SDD) trial to prevent nosocomial pneumonia (NP) during mechanical ventilation (MV), we carried out serial cultures of gastric aspirate to assess the importance of gastric colonization for potential respiratory pathogens and its relationship to the simultaneous gastric pH, to whether the patients were receiving Sucralfate or Ranitidine and to the nutritional biochemical parameters. If NP developed, a bronchial sample was taken by fibreoptic bronchoscopy to determine the causal organisms and its relationship to the previous gastric isolated. Results show: 1) Increase in aerobic Gram negative bacilli colonization during hospitalization. 2) Direct relationship between colonization level and gastric pH. 3) Greater pH in ranitidine vs sucralfate group. 4) Low incidence of NP (11%), the majority of these (66%) being early. 5) No bacteriological correlation between gastric colonization and aetiological agents of NP. 6) Close relationship between pharyngeal colonization and causative germs of pulmonary infection (40%).
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PMID:Role of selective digestive decontamination (SDD) in the prevention of nosocomial pneumonia (NP): is gastric decontamination necessary? 143 May 85

Out of 647 patients with chronic recurrent pancreatitis followed up for 10-12 years 27 patients (4.2%) developed symptomatic gastroduodenal ulcers, 29 (4.5%) multiple gastroduodenal erosions. Ulcers and erosions emerged in patients with pronounced pancreatic bicarbonate insufficiency. Sucralfate treatment produced the best effect, while almagel plus vicalin were superior to gastrozepin. Relapses of ulcerogenesis were registered in 8 cases, multiple erosions in 11 cases, left pleural exudate in 8 cases in the presence of chronic pancreatitis exacerbation. Pancreatocardiac syndrome with cardialgias, a trend to arterial hypotonia, reduced voltage of ECG waves, occasional extrasystolic arrhythmia occurred in 45 patients (7%). It is shown that metabolic disorders of biogenic amines and lowered blood levels of insulin and C-peptide may underlie pathogenesis of pancreatocardiac syndrome.
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PMID:[Course and therapy of nonpancreatic complications of chronic pancreatitis]. 143 94


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