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)

Sucralfate is a nonsystemic agent that is effective in protecting the gastroduodenal mucosa against injury. In addition, sucralfate is effective in the healing of acute duodenal and gastric ulceration, the therapy of esophagitis, and the prevention of ulcer recurrence. The mechanisms responsible for sucralfate's successful protective and therapeutic actions include the adsorption of pepsin and bile acids, the stimulation of bicarbonate and mucus secretion, and stimulation of endogenous synthesis of prostaglandins. When sucralfate is given to experimental animals or humans, it stimulates endogenous synthesis and release of prostaglandin E2 and inhibits thromboxane release. Pretreatment of animals with the cyclooxygenase inhibitor indomethacin results in a marked decrease in the protective effect of sucralfate against alcohol injury. Sucralfate also increases epidermal growth factor binding to ulcerated areas and stimulates macrophage activity. In addition, sucralfate stimulates endogenous sulfhydryl compounds. At the microscopic level sucralfate protects the vascular integrity of the mucosa and the mucosal proliferative zone. It also stimulates epithelial cell restitution and stimulates cell proliferation. The administration of sucralfate before acute injury results in decreased depth and extent of injury and in acceleration of healing. Because of sucralfate's ability to stimulate the protective and reparative mechanisms of the gastric and duodenal mucosa, it is an important nonsystemic agent for the therapy and prevention of peptic ulceration.
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PMID:The protective and therapeutic mechanisms of sucralfate. 219 Mar 4

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

A double blind, randomised, placebo controlled clinical trial was carried out in endoscopically proved chronic duodenal ulcer patients to compare the efficacy of sucralfate and ranitidine. Sucralfate 1 g four times daily and ranitidine 150 mg twice daily were found to be equally effective in inducing ulcer healing (73.1% and 82.1% respectively) during the 6-week treatment period. The rate of recurrence of the ulcer within six months after the initial treatment (84.2% and 82.6%) was also comparable in the sucralfate and ranitidine groups. Sucralfate and ranitidine are equally effective in ulcer healing and prevention of ulcer relapse.
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PMID:Randomised double blind placebo controlled clinical trial of sucralfate and ranitidine in chronic duodenal ulcer. 220 5

Epidermal growth factor (EGF) has been shown to enhance healing of experimental gastric ulcers when given subcutaneously or orally in the drinking water. This effect of EGF occurs without reducing gastric acid secretion. On the other hand, EGF reportedly is excreted rapidly from gastric lumen when administered by intragastric bolus. This suggests that further stimulation of ulcer healing may be expected if EGF is given with an acid-suppressive agent or with an agent allowing EGF to remain in rat gastric lumen at high concentrations. In the present study, EGF administered by gastric intubation at a dose of 10 micrograms/kg, which is three times smaller than reported in previous studies, was evaluated for its effect on acetic acid-induced rat gastric ulcers in combination with sucralfate or omeprazole. Sucralfate is well known selectively to bind proteins covering the ulcer base, and omeprazole is a potent acid-suppressive agent. Prior to the study of combined EGF and sucralfate, oral sucralfate was confirmed to allow endogenous gastric EGF and mouse EGF given exogenously to remain at high concentrations in gastric contents and tissues. EGF and sucralfate (2 g/kg/day) given alone failed to stimulate ulcer healing in submandibularectomized rats (SMR rat) whose endogenous gastric EGF was depleted. However, the combination of both drugs administered at the same doses significantly accelerated ulcer healing in the SMR rat. Omeprazole (200 mg/kg/day) significantly enhanced ulcer healing regardless of removal of the submandibular glands. The combination of EGF and omeprazole further stimulated ulcer healing in the SMR rat.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of epidermal growth factor in combination with sucralfate or omeprazole on the healing of chronic gastric ulcers in the rat. 221 45

A total of 36 patients with grade 2 or greater erosive esophagitis and an abnormal 24-h pH monitor study, were treated in a randomized, double-blind fashion to assess the efficacy of sucralfate suspension as adjunctive therapy to cimetidine for severe esophagitis secondary to gastroesophageal reflux. Treatment consisted of cimetidine, 300 mg qid and either sucralfate suspension (1 g/10 ml) or an identical placebo suspension, 10 ml after meals and 20 ml hs. Patients were treated for 12 wk unless endoscopic healing occurred earlier. Initial evaluation and monthly follow-up consisted of symptom monitoring, endoscopic evaluation and pre- and post-therapy esophageal manometry, Bernstein test, and 24-h pH monitoring. The combination of cimetidine and sucralfate suspension was superior to cimetidine alone in improving daytime heartburn symptoms (p less than 0.05) but not nighttime heartburn, dysphagia, or regurgitation. Sucralfate plus cimetidine improved the overall endoscopic outcome of esophagitis more than cimetidine alone (p less than 0.05). More patients exhibited endoscopic healing in the adjunctive sucralfate group than in the cimetidine-only group. Endoscopic healing, however, was not statistically different between groups. We conclude that sucralfate used as adjunctive therapy to cimetidine resulted in improvement of some of the symptoms of reflux, and probably increases the likelihood of complete healing of esophagitis, compared with cimetidine alone.
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PMID:Sucralfate used as adjunctive therapy in patients with severe erosive peptic esophagitis resulting from gastroesophageal reflux. 222 Jul 25

More than a dozen NSAIDs are commercially available in the United States. Diclofenac may not be as effective for dysmenorrhea. Although most are equally efficacious, indomethacin is the preferred agent for hemicrania continua and chronic paroxysmal hemicrania. Although all NSAIDs should theoretically be beneficial in gout, the greatest experience is with indomethacin. Sulindac may be the preferred agent for diabetic neuropathy. Fenoprofen appears to be the most offensive NSAID in terms of nephrotoxicity. NSAIDs may antagonize antihypertensive therapy, although this effect may not persist beyond 1 month. Generally, use of NSAIDs in pediatric patients is limited to naproxen and tolmetin. Concomitant therapy with methotrexate, lithium, and AZT should be approached with caution. NSAIDs have similar propensities to cause gastrointestinal side effects. Sucralfate has consistently proved beneficial as cytoprotective therapy for use with NSAIDs without impairing absorption of the NSAID, NSAIDs generally should be avoided prior to surgery, although sulindac or nonacetylated salicylates have a negligible effect on platelet function and may be used if continued NSAID therapy is required. Hepatotoxicity, although rare with NSAIDs, is most common with phenylbutazone and least common with the fenamates.
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PMID:Current issues in NSAID therapy. 223 38

To determine the influence of sucralfate on the absorption of erythromycin, prior to evaluating its efficacy in decreasing erythromycin-associated gastrointestinal (GI) intolerance, we assessed pharmacokinetic parameters in six healthy adult volunteers. Erythromycin ethylsuccinate administered alone or with sucralfate as a single dose was compared. Sucralfate did not significantly alter the elimination rate constant, half-life, or area under the curve for erythromycin ethylsuccinate. It is therefore unlikely that efficacy of erythromycin ethylsuccinate will be altered when sucralfate is coadministered.
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PMID:Effect of concurrent sucralfate administration on the absorption of erythromycin. 230 79

Management of acute gastrointestinal bleeding follows a logical sequence of steps. The first priority is to assess the magnitude of blood loss and resuscitate the patient. The patient history and nasogastric aspiration can help localize the source of bleeding to the upper tract or lower tract. Treatment of suspected upper gastrointestinal bleeding is usually empirical and consists of histamine 2 blockers (or sucralfate [Carafate]) or antacids. Diagnosis of the specific bleeding site is based on the severity, activity, and nature of the bleeding. Endoscopic and radiographic techniques may be useful. Intravenous vasopressin (Pitressin) therapy and endoscopic sclerotherapy are important in the management of variceal hemorrhage. Therapeutic endoscopic techniques are being used more often to manage nonvariceal bleeding as well.
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PMID:Acute gastrointestinal bleeding. A logical approach to management. 231 58

The present study evaluated the effect of sucralfate and its components, sucrose octasulfate and aluminum hydroxide, on: (1) damage to rat cultured gastric mucosal cells induced by sodium taurocholate in a neutral environment and in conditions independent of systemic factors, (2) prostaglandin E2 and on 6-keto prostaglandin F1 alpha release by cultured cells, and (3) sulfhydryl content of cultured cells. Cell damage was quantitated by chromium-51 release assay. Prostaglandin E2 and 6-keto prostaglandin F1 alpha were measured by radioimmunoassay. Total sulfhydryl content of cultured cells was determined calorimetrically. Microscopically, sucralfate was found to adhere tightly to epithelial cell surfaces despite frequent washings. Sucralfate 2 mg/ml and 5 mg/ml significantly decreased taurocholate-induced damage, reducing taurocholate-induced specific 51Cr release by 11.8 points (equal to 29% decrease in cell damage, P less than 0.01) and 22.9 points (equal to 56% decrease in cell damage, P less than 0.001), respectively. Sucrose octasulfate and aluminum hydroxide did not exert significant protection against damage induced by sodium taurocholate. The protective effect of sucralfate was not prevented by indomethacin, nor was it counteracted by the sulfhydryl blocker, iodoacetamide. Sucralfate, but not its components, significantly and dose-dependently stimulated prostaglandin E2 (r = 0.94, P less than 0.05) and 6-keto prostaglandin F1 alpha (r = 0.89, P less than 0.05) production by cultured cells. Neither sucralfate nor its components affected sulfhydryl content of cultured cells. In conclusion, sucralfate, but not its components, (1) protects rat gastric mucosal cells against taurocholate-induced damage in conditions independent of systemic factors and in a neutral environment and (2) significantly stimulates prostaglandin production by cultured cells. (3) The protection by sucralfate in vitro does not seem to depend on its stimulatory effect on endogenous prostaglandin synthesis.
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PMID:Effect of sucralfate and its components on taurocholate-induced damage to rat gastric mucosal cells in tissue culture. 231 93

1. Sucralfate (basic sucrose aluminium sulphate), a topical intestinal agent, was administered in suspension or granule form to 25 healthy subjects at a total dose of 4 g day-1 for 21 days. Aluminium in plasma and 24 h urine samples was assayed before, during and after administration of sucralfate by inductively coupled plasma optical emission spectrometry. 2. Sucralfate produced significant increases in plasma and urine aluminium concentrations. On average, plasma aluminium increased from about 2 micrograms 1-1 to more than 5 micrograms 1-1 and 24 h urine aluminium increased from less than 5 micrograms to more than 30 micrograms. Both plasma and urine aluminium concentrations decreased rapidly after sucralfate was stopped. However, urinary aluminium concentrations remained higher than normal 5 and 10 days after discontinuation of sucralfate administration. Moreover subjects receiving sucralfate granules had significantly higher average urinary excretion of aluminium than subjects receiving the suspension. 3. The small but significant increase in plasma and urine aluminium following sucralfate administration in therapeutic doses may reflect intestinal absorption of aluminium. Although such absorption would appear to be moderate in healthy subjects, it is suggested that aluminium-based treatments should be used only intermittently, especially in patients with renal disorders.
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PMID:Plasma and urine aluminium concentrations in healthy subjects after administration of sucralfate. 195 83


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