Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

As many as 72 patients with erosive and ulcerous injuries to the stomach and duodenum were examined for the clinical efficacy of antepsin (sucralfate). Of these patients, 42 were with duodenal ulcer, 10 with gastric ulcer and 20 with erosive gastroduodenitis). Antepsin exerted a beneficial effect on the painful syndrome and on ulcer and erosion healing. The coefficient of the therapeutic efficacy of antepsin in duodenal ulcer patients turned out to be equal to 2.67 that of gastric ulcer to 2.1 and that in patients with gastroduodenitis was 2.6. The drug did not produce any well-defined side effects. In some cases (8.3%), it caused the appearance or enhancement of constipation. Antepsin is indicated not only in ulcer disease but also in duodenogastric reflux, reflux gastritis and reflux esophagitis.
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PMID:[Sucralfate: the agent of choice in the treatment of peptic ulcer?]. 218 96

Pharmacokinetics, metabolism, and binding capability of a basic aluminium salt of sucrose octasulphate (sucralfate, Ulcogant) to ulcer lesions were investigated in Wistar rat, Beagle dog, Rhesus, and Cynomolgus monkey with 14C-labelled material. After i.v. injection in rats the 14C-radioactivity has a very short serum half-life of 1 h and is excreted almost completely by the kidneys. After oral administration only a very small portion of the dose is detectable in serum which is eliminated rapidly from the intravascular space. From the renal excretion data it is concluded that sucralfate is absorbed from the gastrointestinal tract of rat, Beagle dog, and Rhesus monkey only from 1% to 5% of the dose. The radioactive constituents in plasma, urine, and feces of rat and Cynomolgus monkey were analysed by HPLC. Both after i.v. and p.o. administration only unchanged substance could be detected. A possible binding of 14C-sucralfate to the ulcerated mucosa of stomach and duodenum was investigated in rats by histoautoradiography. The ulcers were induced by acetic acid. A selective accumulation of 14C-sucralfate in the area of the stomach ulcer could be demonstrated as long as 8 h after single p.o. administration. In the duodenum the autoradiographs showed a specific binding of 14C-sucralfate to the ulcerated mucosa at 1, 2, and 4 h after administration. Neither pretreatment with an H2-receptor antagonist nor simultaneous administration of an antacid influenced the binding of 14C-sucralfate. These results suggest that the mode of action of sucralfate is the formation of a protective layer which stops harmful agents like gastric juice and bile from further damaging the ulcerous lesions, thus ensuring an uninterrupted healing process. The very small extent of absorption and the rapid excretion from the organism minimize the risk of a systemic burden.
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PMID:Sucralfate: pharmacokinetics, metabolism and selective binding to experimental gastric and duodenal ulcers in animals. 689 47