Sucralfate is only minimally absorbed from the gastrointestinal tract. The small amounts of the sulfated disaccharide that are absorbed are excreted primarily in the urine.

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. The following observations also appear pertinent:

1. Studies in human subjects and with animal models of ulcer disease have shown that sucralfate forms an ulcer-adherent complex with proteinaceous exudate at the ulcer site.
2. In vitro, a sucralfate-albumin film provides a barrier to diffusion of hydrogen ions.
3. In human subjects, sucralfate given in doses recommended for ulcer therapy inhibits pepsin activity in gastric juice by 32%.
4. In vitro, sucralfate adsorbs bile salts.

These observations suggest that sucralfate's antiulcer activity is the result of formation of an ulcer-adherent complex that covers the ulcer site and protects it against further attack by acid, pepsin, and bile salts. There are approximately 14 to 16 mEq of acid-neutralizing capacity per 1-g dose of sucralfate.

Clinical Trails

In a multicenter, double-blind, placebo-controlled study of CARAFATE Suspension, a dosage regiment of 1 g (10 mL) four times daily was demonstrated to be superior to placebo in ulcer healing.

Results From Clinical Trials Healing Rates for Acute Duodenal Ulcer

Equivalence of sucralfate suspension to sucralfate tablets has not been demonstrated.

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