Gastroprotection by sucralfate against acetylsalicylic acid in humans. Role of endogenous prostaglandins.

Sucralfate has been shown to prevent the formation of acute gastric lesions induced by nonsteroidal antiinflammatory drugs such as aspirin (ASA) in animals, but little is known about the prevention by this agent of ASA-induced gastric damage in humans. This report describes the effects of sucralfate on mucosal formation of prostaglandins (PG), gastric microbleeding and DNA loss in intact and ASA-challenged stomach. Two groups of 12 healthy volunteers were used in a double-blind, placebo controlled trial to assess the effects of sucralfate 1.0g qid on the stomach in subjects without (group A) and with administration of 2.5g ASA during 2 days (group B). Sucralfate treatment during 4 days significantly reduced spontaneous gastric bleeding and DNA loss in group A and prevented blood loss caused by ASA in group B. The protective effects of sucralfate on spontaneous gastric blood loss were accompanied by increased mucosal biosynthesis and luminal release of PGE2 and 6-keto-PGF1 alpha with decreased release of TXB2. In ASA-treated subjects mucosal generation and luminal release of PG and TXB2 were greatly suppressed and sucralfate treatment did not influence these PGs in spite of the decreased mucosal damage. It is concluded that sucralfate has a potent protective action on spontaneous and ASA-treated gastric bleeding in man and that this protection may be partly due to the increased mucosal biosynthesis of prostaglandins.