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For the short-term treatment (up to 8 weeks) of active duodenal ulcer, as well as maintenance therapy for duodenal ulcer patients at reduced dosage (1 gram twice a day) after healing of acute ulcers. Also used for the short-term treatment of gastric ulcer.
Although sucralfate's mechanism is not entirely understood, there are several factors that most likely contribute to its action. Sucralfate, with its strong negative charge, binds to exposed positively-charged proteins at the base of ulcers. In this way, it coats the ulcer and forms a physical barrier that protects the ulcer surface from further injury by acid and pepsin. It directly inhibits pepsin (an enzyme that breaks apart proteins) in the presence of stomach acid and binds bile salts coming from the liver via the bile thus protecting the stomach lining from injury caused by the bile acids. Sucralfate may increase prostaglandin production. Prostaglandins are known to protect the lining of the stomach and may also bind epithelial growth factor and fibroblast growth factor, both of which enhance the growth and repair mechanism of the stomach lining.
Acute oral toxicity (LD<sub>50</sub>) in mice is >8000 mg/kg. There is limited experience in humans with overdosage of sucralfate. Sucralfate is only minimally absorbed from the gastrointestinal tract and thus risks associated with acute overdosage should be minimal. In rare reports describing sucralfate overdose, most patients remained asymptomatic.
Minimally absorbed from the gastrointestinal tract (up to 5% of the disaccharide component and less than 0.02% of aluminum).
Not known.
The small amounts of the sulfated disaccharide that are absorbed are excreted primarily in the urine.