Brands, Medical Use, Clinical Data
- Tablet for oral administration (1g)
Brands / Synonyms
Antepsin; Apo-sucralfate; Carafate; Carafate Suspension; Sulcrate; Sulcrate Suspension Plus; Ulcar; Ulcerban; Ulcerlmin; Ulcogant
For the short-term treatment (up to 8 weeks) of active duodenal ulcer. Also used as maintenance therapy for duodenal ulcer patients at reduced dosage (1 gram twice a day) after healing of acute ulcers.
Sucralfate is a prescription medication used to treat peptic ulcers. The current clinical uses of sucralfate are limited. It is effective for the healing of duodenal ulcers, but it is not frequently used for this since more effective drugs (e.g. proton pump inhibitors) have been developed. Although the mechanism of sucralfate's ability to accelerate healing of duodenal ulcers remains to be fully defined, it is known that it exerts its effect through a local, rather than systemic, action. Chemically, sucralfate is a complex of the disaccharide sugar, sucrose, combined with sulfate and aluminum. In acidic solutions (e.g. gastric acid) it forms a thick paste that has a strong negative charge.
Mechanism of Action
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, and 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.
Minimally absorbed from the gastrointestinal tract (up to 5% of the disaccharide component and less than 0.02% of aluminum).
Acute oral toxicity (LD50) 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.
Biotrnasformation / Drug Metabolism
There are no known contraindications to the use of sucralfate.
Some studies have shown that simultaneous sucralfate administration in healthy volunteers reduced the extent of
absorption (bioavailability) of single doses of the following: cimetidine, digoxin, fluoroquinolone antibiotics,
ketoconazole, l-thyroxine, phenytoin, quinidine, ranitidine, tetracycline, and theophylline. Subtherapeutic
prothrombin times with concomitant warfarin and sucralfate therapy have been reported in spontaneous and published
case reports. However, two clinical studies have demonstrated no change in either serum warfarin concentration or
prothrombin time with the addition of sucralfate to chronic warfarin therapy.
The mechanism of these interactions appears to be nonsystemic in nature, presumably resulting from sucralfate
binding to the concomitant agent in the gastrointestinal tract. In all cases studied to date (cimetidine,
ciprofloxacin, digoxin, norfloxacin, ofloxacin, and ranitidine), dosing the concomitant medication 2 hours before
sucralfate eliminated the interaction. Because of the potential of CARAFATE to alter the absorption of some drugs,
CARAFATE should be administered separately from other drugs when alterations in bioavailability are felt to be
critical. In these cases, patients should be monitored appropriately.