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

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

Drugs used in the treatment of peptic ulcer disease may interact with the renal system in a variety of ways. Since many agents are eliminated by renal excretion, clearance of these agents may be reduced and half-life extended in the presence of renal insufficiency. The histamine H2-receptor antagonists may interfere with renal tubular excretion of creatinine and cationic drugs, resulting in elevated serum concentrations and reduced renal clearance. The prostaglandin E1 analogue misoprostol is used as a cytoprotective agent but has renal effects. The renal effects differ between systems studied. In the rat, misoprostol reduces cyclosporin-induced renal tubular toxicity, whereas in humans it has been shown to attenuate renal allograft rejection. Sucralfate is the aluminium salt of sucrose octasulfate. It permits the absorption of aluminium in amounts similar to aluminium-containing antacids, and toxicity has been demonstrated in the presence of renal insufficiency. Bismuth compounds are used increasingly to treat peptic ulcer disease, and bismuth toxicity has been described in association with renal insufficiency. Aluminium-, calcium- and magnesium-containing antacids are used as oral phosphate binders in patients with renal insufficiency in addition to their usual indications. Cation absorption and accumulation with all of these antacid preparations has been described and may lead to toxicity.
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PMID:Renal effects of peptic ulcer therapy. 152

Sucralfate, a basic aluminum salt of sucrose, was the first successful drug with a major cytoprotective mechanism of action. It binds bile acids and pepsin and adheres to both ulcerated and nonulcerated mucosa. Sucralfate stimulates the synthesis and release of gastric mucosal prostaglandins as well as bicarbonate and the epidermal growth factor which stimulates healing. Sucralfate is the safest drug available today in the treatment of dyspeptic symptoms and compared to ranitidine and cimetidine it has the following characteristics. (2) The short-term healing of duodenal ulcers is the same for sucralfate, cimetidine and ranitidine. (3) Sucralfate-treated patients have a lower recurrence rate of duodenal ulceration after healing when compared with cimetidine and the recurrence rate is not connected with the presence or absence of Campylobacter pylori.
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PMID:Role of sucralfate in peptic disease. 161 11

Over the past 5-10 years, a number of studies have shown that topical sucralfate enhances a number of gastric and duodenal mechanisms, e.g., the "mucus-bicarbonate barrier," mucosal hydrophobicity, mucosal blood flow, cell viability, and local production of prostaglandins, as well as endogenous mediators of tissue injury and repair. It seems likely that the complex actions of sucralfate are in part related to direct interaction between the drug or its components (aluminum, sucrose, and sulfate) and gastric mucosal tissues, and in part related to effects of the drug on the various mucosal mediators of tissue injury and repair. Local actions may play a role in accelerating healing of ulcer-damaged mucosa, but this does not explain the protective actions of sucralfate on normal mucosa. Thus sucralfate appears to enhance the protective function of the "mucus-bicarbonate" barrier by actions on both components. This may depend in part on an interaction with the unstirred layer overlying gastric epithelium. Sucralfate has also been shown to increase the hydrophobicity of mucus gel. There is little doubt that sucralfate increases local production and release of protective prostaglandins (PGs), but the precise role played by these agents in mediating mucosal protection and in chronic ulcer healing remains uncertain. Currently, the mechanism of action of sucralfate on vascular integrity remains unknown and the role of PGs in this protective function is unclear. There is little evidence that epidermal growth factor plays any role in mediating mucosal protection by sucralfate, but it may be important in its ulcer-healing action. Sucralfate has been shown to be truly "cytoprotective" in that it protects isolated epithelial cells from damage by noxious agents. In animals treated with sucralfate, the surface epithelial cells were disrupted, but necrotic lesions in the deep proliferative zone were virtually absent. It seems likely that investigations of the actions of sucralfate and its components will move ever closer to defining the target cells, the intracellular events, and the mediators that bring about its protective and ulcer-healing activity.
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PMID:Mechanisms of gastroduodenal protection by sucralfate. 171 73

Sucralfate, an aluminum salt of sucrose octasulfate, has been shown to be effective in reducing the discomfort of radiation therapy-induced oral mucositis. This study was done to determine whether sucralfate could be used as a nutritional source for dental caries-producing organisms. Three Streptococcus strains were cultured in a defined medium. Sucralfate powder was evaluated for its ability to be used as a carbohydrate food source by these organisms. The addition of sucralfate alone did not stimulate the organism's growth. The addition of sucralfate and glucose resulted in less growth than the addition of glucose alone. Increasing the sucralfate concentration from 1% to 10% in the glucose-containing cultures resulted in statistically significant growth inhibition (p less than 0.02). Sucralfate appears to have no cariogenic potential and may have some cariostatic potential.
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PMID:The effect of sucralfate on the growth of cariogenic streptococci. 177 88

Sucralfate, an aluminum hydroxide complex of sulfated sucrose used in the treatment of gastric ulcer, was shown to prevent irradiation-induced diarrhea and bowel discomfort significantly in patients treated for pelvic cancer with external radiotherapy with intent to cure. The double-blind placebo-controlled study included 70 patients with carcinoma of the prostate and urinary bladder without distant metastasis (T1-4NO1xMO) and performance status of greater than or equal to 90% Karnofsky scale. Radiotherapy was administered in a conventional manner with MeV photons and a four-field technique. The total dose was 62-66 Gy and total treatment time of 6.5 weeks. Dose granules of sucralfate or placebo were dispensed to each patient 2 weeks after radiation started and continued for 6 weeks. All analyses were performed blindly. Seven of 34 evaluable patients in the placebo group and 18 of 32 evaluable patients in the sucralfate group did not present with diarrhea during the observation period. The frequency of defecation and stool consistency were significantly improved by sucralfate. Fourteen patients in the placebo group and only three in the sucralfate group required symptomatic therapy with loperamide. There was no evidence of adverse effects associated with the use of sucralfate. Sucralfate can be of beneficial value in diminishing the bowel discomfort during radiotherapy of pelvic malignancies, and the earlier proposed mechanisms of action (e.g., protection of denuded mucosa, cytoprotective properties, binding bile acids) can also be valid for the current effects of sucralfate.
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PMID:Prevention of irradiation-induced bowel discomfort by sucralfate: a double-blind, placebo-controlled study when treating localized pelvic cancer. 188 3

Viable bacteria in the gut of thermally injured patients may be translocated through the gut mucosa, causing widespread infection. Increased flora from optimization of bacterial growth by pH elevation, coupled with the decreased intestinal motility common among patients whose mucosal integrity has been compromised, may increase the incidence of translocation. Gastric pH in these patients is monitored and maintained around pH 6 by various agents to reduce susceptibility to stress ulceration. Whole milk, given as a nutrient source, also raises pH. An in vitro trial simulating gastric fluid under conditions found in patients with burns was conducted to evaluate the growth of commonly ingested bacteria. Bicarbonate buffer containing pepsin and adjusted to pH 2, 4, or 7 with HCl was dosed with magnesium and aluminum hydroxide antacid (Maalox) (10 ml), sucralfate (Carafate) (0.4 gm), or prostaglandin E2 (PGE2) (10 ng) before inoculation with Escherichia coli (3 x 10(2) organisms), Pseudomonas aeruginosa (3 x 10(2) organisms), or Staphylococcus aureus (2 x 10(1) organisms). Bacterial growth and pH were determined periodically over the 24-hour trial. Milk was added at intervals in half the samples to simulate patient feeding. Maalox increased pH in all samples containing milk (initially pH 2, 4, or 7) to over 7.0 in 2 hours, and increased pH more slowly without milk. Carafate had a moderating effect, increasing pH 2 and pH 4 and decreasing pH 7, with a narrower pH range found in the milk groups. PGE2 treatments combined with milk also increased pH 2 and pH 4, but slightly elevated pH 7 within 24 hours. Without milk, PGE2 did not alter pH from initial values.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antacid, sucralfate, and prostaglandin E2 effects on the growth and potential for translocation of Pseudomonas aeruginosa, Escherichia coli, and Staphylococcus aureus in an in vitro gastric simulation. 190 78

A method producing persistent gastric ulcers in the rhesus monkey by combined mucosal injury and gamma-irradiation was modified and evaluated in the rabbit. gamma-Irradiation (800-1000 cGy) immediately after removal of 2-mm-diameter sections of antral mucosa resulted in ulcer craters 5-7 days later. Ulcer sites were characterized by loss of the mucosa, muscularis mucosa, and much of the submucosa. The exposed submucosa was coated with fibrin and necrotic debris infiltrated with heterophils, the rabbit equivalent of neutrophils. These ulcers strongly resemble human chronic gastric ulcers. Binding of Carafate (sucralfate; Marion Laboratories, Inc., Kansas City, MO) and Maalox (magnesia-alumina oral suspension; Wm. H. Rorer, Inc., Ft. Washington, PA) to ulcer and nearby nonulcer sites in the antrum was assessed 1 hour after drug dosing. Drug binding was determined by aluminum quantitation of stomach wall punch biopsies at necropsy. Both drugs significantly increased aluminum bound to the stomach wall compared with vehicle treatment. Significantly more antiulcer drug was bound to ulcer sites than to nearby nonulcer sites only after sucralfate administration. This model of persistent gastric ulcer should be useful to further study gastric ulcer pathogenesis and treatment.
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PMID:Mucosal injury and gamma-irradiation produce persistent gastric ulcers in the rabbit. Evaluation of antiulcer drug binding to experimental ulcer sites. 201 69

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


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