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 use of non-prescription antacids to control hyperphosphatemia has been implicated as a primary cause of aluminum intoxications in patients with reduced renal function. Additional reports suggest that oral aluminum intake may have adverse effects on mineral metabolism of patients with normal renal function. The non-prescription drugs that contain substantial quantities of aluminum salts include some antacids, buffered aspirins, antidiarrheals, and vaginal douches. Sucralfate, an anti-ulcer drug available by prescription, is the aluminum salt of sucrose sulfate. If taken as directed, the daily aluminum intake from the antacids can be as much as 5,000 mg. When aluminum buffered aspirins are used as part of the drug therapy for rheumatoid arthritis, aluminum intake can be elevated by 700 mg/day. Although aluminum intoxications have been reported among patients with reduced renal function, existing reports are not sufficient to estimate whether the chronic elevation of aluminum intake from drugs is causing adverse health effects among other patient populations.
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PMID:Aluminum intake from non-prescription drugs and sucralfate. 383 82

Sucralfate is a basic aluminium salt of sulphated sucrose which is advocated for use in peptic ulcer disease. It is minimally absorbed after oral administration and is believed to act primarily at the ulcer site by protecting the ulcer from the effects of pepsin, acid and possibly bile salts. Controlled therapeutic trials have demonstrated that sucralfate 1g 4 times daily is effective in increasing the rate of healing of duodenal and gastric ulcer over a period of 4 to 8 weeks. Trials comparing sucralfate and cimetidine have not found any significant difference in efficacy between the drugs in small numbers of patients. A dosage of 2g daily given prophylactically decreases the rate of recurrence of duodenal ulcers, but the efficacy of sucralfate in preventing relapse of gastric ulcers has yet to be clearly demonstrated. Sucralfate is particularly well tolerated. Constipation, the most common side effect, occurs in 2% of patients. Thus, sucralfate offers an effective and well tolerated alternative for the management of peptic ulcer disease.
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PMID:Sucralfate. A review of its pharmacodynamic properties and therapeutic use in peptic ulcer disease. 636 84

The treatment of peptic ulcer disease has been revolutionized for both the physician and the surgeon by the development of the histamine H2-antagonists, which have become the 'gold standard' for peptic ulcer therapy. However, it has been shown that several other drugs, including antacids, can match the ulcer-healing rate obtained with histamine H2-antagonist therapy with both a high- and a low-dose regimen. An important and well-documented option is the treatment of peptic ulcer disease with sucralfate. This drug, a basic amino salt of sucrose octosulphate , acts by binding to the protein of the matrix of the ulcer crater, thus coating the ulcer against the aggressive principle of acid-pepsin and probably also by a cytoprotective effect. Sucralfate is only absorbed in minimal quantities and no metabolic interaction with other drugs is therefore likely to occur. In many studies performed on different continents it has been demonstrated that sucralfate is superior to placebo in short-term duodenal and gastric ulcer healing and that the rate of healing is similar to that obtained by cimetidine. Evidence is also accumulating that sucralfate has a place in maintenance therapy to prevent recurrence of duodenal ulcer; preliminary studies also point to benefit in the therapy of reflux oesophagitis.
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PMID:The other option in peptic ulcer therapy. 637 32

Acid and pepsin have been designated the "aggressive factors" in peptic ulcer because they are essential for ulcer formation and because a reduction in their luminal concentrations is usually followed by ulcer healing. Acid enables peptic aggression by converting pepsinogen to pepsin, by providing the highly acidic pH required for pepsin activity, and by denaturing proteins, thereby increasing their susceptibility to the action of pepsin. Pepsin causes peptic aggression by hydrolyzing peptide linkages which bind together the constituent amino acids of proteins. The first step in this reaction is the formation of a complex between the active site of pepsin and the protein substrate. Sucralfate, which is the basic aluminum salt of sucrose octasulfate, inhibits this step by forming an electrostatic complex with proteins. As such, sucralfate inhibits peptic aggression without decreasing acid-pepsinogen secretion or raising intragastric pH. Because of its affinity for proteins and its insolubility and inherent viscosity in acid, sucralfate forms a physical coating over the ulcer crater. This coating further inhibits peptic aggression by producing a barrier to the diffusion of acid and pepsin. Additionally, the basic aluminum moieties of sucralfate may serve to buffer hydrogen ions as they attempt to permeate the viscous layer. The sum of these effects appears to explain the ability of sucralfate to accelerate the rate of healing of peptic ulcer.
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PMID:Inhibition of peptic aggression by sucralfate. The view from the ulcer crater. 641 6

Sucralfate, an aluminum salt of sulfated sucrose, is a new drug designed for the treatment of peptic ulcer. Sucralfate has been reported to be useful in a variety of situations including prevention of aspirin-induced gastric mucosal damage. We investigated the in vitro adsorption of bile salts or aspirin to sucralfate in environments simulating the stomach (pH 1.5), small intestine (pH 7), and colon (pH 7.8). Bile salts were incubated with sucralfate, and the quantity of bile salt adsorbed was calculated by subtraction from the amount remaining in solution after centrifugation at 12,500g for 30 min. Adsorption experiments were performed in bile salt solutions at pH 1.5 and 7.0 with 0-10 g/dl sucralfate using glycocholate, glycochenodeoxycholate, taurocholate, taurodeoxycholate, or taurochenodeoxycholate. The dihydroxy-unconjugated bile salts, deoxycholic, and chenodeoxycholic salts were tested at pH 7.8. Binding capacity (micromoles per gram sucralfate) was calculated from the linear regression of micromoles bound vs grams sucralfate incubated. Sucralfate adsorbed all bile salts tested (except taurocholic acid at pH 1.5) but was less effective than cholestyramine. Sucralfate does not adsorb sufficient bile salts at neutral pH to cause bile salt depletion. Aspirin was minimally adsorbed by sucralfate [7.5 mumol (1.4 mg)/g sucralfate, pH 1.5], and thus adsorption of aspirin does not explain the protective effect of sucralfate against aspirin injury.
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PMID:In vitro adsorption of bile salts and aspirin to sucralfate. 654 15

The effects of oral sucralfate, a basic aluminum salt of sulfated disaccharide, on various experimental gastric lesions and on gastric secretion were studied in rats. Sucralfate at 300 mg/kg potently inhibited the development of Shay ulcers and indomethacin- and aspirin-induced erosions. The drug at 1000 mg/kg also potently inhibited histamine-induced erosions. Water-immersion stress-induced erosions were inhibited with 1000 mg/kg of the drug, but the degree of inhibition was weaker than that seen in other types of erosion formation. Sucralfate at 1000 mg/kg given twice daily for 14 days significantly accelerated the spontaneous healing of acetic acid-induced ulcers. Sucralfate at over 300 mg/kg tended to increase the volume of gastric juice but had an insignificant effect on acid and pepsin output of pylorus-ligated rats. As a whole, the effects of sucralfate on experimental gastric lesions appear to be much more potent than Maalox, propantheline bromide, and cimetidine. The mechanism of action of sucralfate remains to be determined.
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PMID:Effects of an antiulcer drug, sucralfate (a basic aluminum salt of sulfated disaccharide), on experimental gastric lesions and gastric secretion in rats. 668 79

Sucralfate, a basic aluminum salt of sucrose octasulfate, was developed to counteract the activities of both acid and pepsin. It differs chemically from other sulfated anionic inhibitors of pepsin in being a base and a derivative of pure disaccharide sucrose. The development of sucralfate was guided by the observations that sulfated disaccharides do not exhibit the anticoagulant activity of sulfated polysaccharides, and that the inhibition of peptic activity and the protection against experimental ulceration depend only on the degree of sulfation. Sucralfate has been found to protect pylorusligated animals from peptic ulceration more effectively than a mixture of sucrose octasulfate and aluminum hydroxide. Sucralfate has several unusual properties. On encountering gastric acid, it becomes a highly condensed, viscous substance with the capacity to buffer acid. These properties are retained in the duodenum. Sucralfate forms stable complexes with proteins and inhibits their hydrolysis by preventing pepsin-substrate interaction. Sucralfate also inhibits peptic activities by direct adsorption of pepsin. In addition, sucralfate adsorbs bile salts. The sum of these properties implies that sucralfate provides a comprehensive defense against identified aggressive factors, acid, pepsin, and bile salts.
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PMID:Development and characteristics of sucralfate. 679 99

14C-Sucralfate, a basic aluminum salt of 14C-sucrose sulfate, or potassium 14C-sucrose sulfate was administered orally to rats with acetic acid-induced gastric ulcer. The radioactivities representing specific binding of the sucrose sulfate moiety were found significantly higher in ulcer sections of the stomach, with the mean within-animal ulcer/non-ulcer ratio attaining 6, 7, 12 and 2.5, respectively, at 1, 3, 6 and 24 h after 14C-sucralfate administration. Microautoradiography provided direct in vivo evidence for binding of the 14C-sucrose sulfate moiety to exuded proteins resulting in effect in formation of a pepsin-resistant barrier over the surface of an ulcer crater. No comparable findings were obtained in the area of normal mucosa. The administration of 14C-sucralfate was associated with much greater and longer-sustained binding to the ulcer lesion and retention in the stomach and duodenum than simple administration of the soluble potassium salt. These findings not only demonstrate therapeutically significant effects of basic aluminum compoundation but also substantiate likely differences from pepsin inhibitors such as amylopectin sulfate in terms of presence or absence of adhesiveness, local barrier effects, and long duration of actions.
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PMID:Selective binding of sucralfate to ulcer lesion. II. Experiments in rats with gastric ulcer receiving 14C-sucralfate or potassium 14C-sucrose sulfate. 689 77

Sucralfate is a basic aluminum salt of a sulfated disaccharide. In this study, patients with gastric ulcer were given oral multiple doses of sucralfate prior to partial gastrectomy, and binding of the drug to the ulcer lesion and to nonulcerated mucosa was estimated by chemical determination of aluminum and sulfated disaccharide. The ulcerated mucosa was found to contain, on the average, 6-7 times more sucralfate per square centimeter than the control mucosa (P less than 0.01 and less than 0.05 for aluminum and sulfated disaccharide, respectively). The high affinity of sucralfate for ulcerated mucosa, particularly the sucrose sulfate moiety, supports previous data that the beneficial effect of sucralfate in ulcer disease is due in part to complex formation between sucrose sulfate and proteins at the ulcer site.
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PMID:Selective binding of sucralfate to gastric ulcer in man. 689 71

Sucralfate, a basic aluminum salt of sucrose sulfate, has been shown to accelerate the healing of peptic ulcers. We studied its binding to normal and ulcerated rat mucosa after gastric and duodenal ulcers had been induced by acetic acid. Sucralfate adhered to ulcerated mucosa for over 6 hours, in the presence and absence of antacid. Food, eaten 1 hour after sucralfate administration, did not appear to alter its selective binding to ulcer sites, but did reduce the amount of sucralfate bound to healthy tissue. The results suggest that sucralfate has a greater affinity for ulcerated mucosa than normal mucosa.
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PMID:Effect of food and antacid on binding of sucralfate to normal and ulcerated gastric and duodenal mucosa in rats. 689 42


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