Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
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.
 ...
PMID:Sucralfate: antipeptic, antiulcer activities and antagonism of gastric emptying. 38 45

In 1984 Roark published the first report of a sucralfate treatment of esophageal ulcers after sclerotherapy. Because this was an uncontrolled trial we planned a prospective double-blind placebo-controlled study with 60 patients. After therapeutic paravariceal injection-sclerotherapy of esophageal varices, patients were randomly treated with sucralfate suspension or placebo. Time of treatment was limited to a maximum of 3 weeks and the dosage of sucralfate was 1 g q.i.d. (Ulcogant-Suspension). Healing was assessed by endoscopy at weekly intervals. Fifty-three patients (25 sucralfate, 28 placebo) were evaluable according to the protocol. No patient left the study because of side effects. At the start of the trial, the patients in the sucralfate group showed a larger ulcer area than the placebo group. There was a tendency to faster healing in the sucralfate group, especially in patients with deeper ulcerations. However, there was no significant difference in global healing between both treatment groups after 3 weeks. Sucralfate suspension may be of value in accelerating the healing process in esophageal ulcers after sclerotherapy, especially in patients with deep ulcers. These results should be confirmed in further trials, in which patients should be stratified with respect to their ulcer volume and severity of liver disease.
 ...
PMID:A comparison of sucralfate with placebo in the treatment of esophageal ulcers following therapeutic endoscopic sclerotherapy of esophageal varices--a prospective controlled randomized trial. 188 1

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)
 ...
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.
 ...
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 mucosal protective effect of sucralfate (Ulcogant) was evaluated in a prospective randomised clinical study during radiation therapy. Twenty-four patients received 1 g of a sucralfate suspension 4 times a day orally for 5 min each. This group was compared with a control group of 21 patients receiving standard oral hygiene consisting of frequent tooth cleaning and disinfection of the oral and pharyngeal mucosa. The radiation technique was telecobalt therapy in two opposing fields using the shrinking field technique, with an electron boost to the posterior lymph nodes; the dosage was 60-70 Gy in daily fractions of 2 Gy. Mucosal reactions, pain and difficulty in swallowing were recorded twice a week. We also checked the patient's weight during treatment. The patients showed significant differences in all parameters, and lower weight loss compared with the control group. Minimal or absent mucosal inflammation pain or dysphagia were found in 88%, 79% and 83% respectively, while 43% and 29% and 52% of the controls had such mild radiation side-effects. Local effectivity appeared to be less in the hypopharynx due to shorter time of application compared with mouth and oropharynx. There were no side-effects from the sucralfate. Sucralfate prophylaxis is effective and easy to apply in the protection of mucosa during irradiation therapy.
 ...
PMID:[Radiotherapy of head-neck neoplasms: prevention of inflammation of the mucosa by sucralfate treatment]. 217 76

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.
 ...
PMID:Acute gastrointestinal bleeding. A logical approach to management. 231 58

We have validated a method to measure bile salt binding by Maalox (aluminum hydroxide and magnesium hydroxide), Carafate (sucralfate), and Questran (cholestyramine) in vitro. The method used in this study involves a correction for adherent water volume and thus provides a correct measure of bile salt binding. With this approach, we described the binding properties of Maalox, Carafate, and Questran. The bile salt binding capacities of Carafate and Maalox are limited and do not have physiological or pharmacological significance. On the other hand, we found that Questran has substantial bile salt binding capacity. At the recommended dosage, Questran could deplete the total bile salt pool. We also found that Carafate, although not used as an antacid, has buffering capacity (maintaining a pH of solution in the range 4.2-4.8) which might contribute to its effectiveness as an ulcer treatment drug.
 ...
PMID:Bile salt binding properties of commonly used gastrointestinal drugs: maalox, carafate, and questran. 317 34

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.
 ...
PMID:Efficacy of sucralfate and cimetidine in protection of the human gastric mucosa against alcohol injury. 366 9

Sucralfate (Carafate) is a new anti-ulcer agent the effects of which are mediated locally in the gastrointestinal tract. The use of this compound in conjunction with ulcerogenic drugs such as ibuprofen may represent a means of reducing gastrointestinal irritation. Combined oral therapy, however, requires evaluation of a potential interaction in absorption between those agents. The purpose of this study was to examine the influence of sucralfate coingestion on ibuprofen absorption. Twelve normal, healthy male subjects ingested a single oral 400 mg dose of ibuprofen alone or with sucralfate given as 1 g doses four times a day for 2 days prior to and during the study. Ibuprofen serum concentrations were measured for 12 hours following dosing. Parameters associated with rate of absorption (i.e. Cmax, tmax, Ka) were significantly altered in the presence of sucralfate (p less than 0.05). In contrast, the relative bioavailability of ibuprofen was not significantly different between treatments (p greater than 0.05). Therefore, sucralfate does not alter the extent of ibuprofen absorption and would not be expected to change the response to that anti-inflammatory agent.
 ...
PMID:The influence of sucralfate on ibuprofen absorption in healthy adult males. 377 35

The pharmacology, pharmacokinetics, clinical studies, adverse reactions, and dosage of sucralfate (Carafate, Marion Laboratories), a unique drug for peptic-ulcer disease, are reviewed. Sucralfate exerts its antiulcer effect by binding with proteinacious material, neutralizing local acidity without affecting gastric pH, and forming a protective barrier at the ulcer site. It also inhibits the diffusion of hydrogen ion, inhibits the action of pepsin, and adsorbs bile salts. Approximately 3-5% of an orally administered dose of sucralfate is absorbed; more than 90% of the dose is excreted unchanged in the feces. Sucralfate remains at the site of gastric ulcers for up to six hours. In the treatment of duodenal ulcers, sucralfate is more effective than placebo and comparable with cimetidine and intensive antacid therapy. Healing rates for gastric ulcers are less impressive but are comparable with those produced by cimetidine and antacids. Additive or synergistic effects of sucralfate with cimetidine or intensive antacid therapy have not been studied. Sucralfate has few side effects because it is not absorbed; most frequently reported are constipation (3-4%), xerostomia (1%), and skin eruptions (0.6%). No drug-drug interactions have been reported. The recommended dose of sucralfate is 1 g four times a day one hour before meals and at bedtime. Sucralfate is a unique antiulcer drug that compares favorably with cimetidine and antacid therapy in terms of safety and efficacy. Sucralfate is FDA-approved for short-term (up to eight weeks) treatment of duodenal ulcers.
 ...
PMID:Sucralfate--alternative therapy for peptic-ulcer disease. 676 89


1 2 Next >>