Effect of synthetic 15-methyl analog of PGE2 on gastric acid and serum gastrin response to peptone meal, pentagastrin, and histamine in duodenal ulcer patients.

Abstract

The effect of 15(S)-15-methyl PGE2, methyl ester (15-ME-PGE2), used intravenously in a standard dose of 0.5 mug/kg-hr on gastric secretion and serum gastrin level was studied in 6 duodenal ulcer patients. 15-Me-PGE2 caused an immediate and almost complete inhibition of basal gastric acid and pepsin secretion. Acid secretion induced by a peptone meal and determined by intragastric titration technique was almost as high as the maximal response to histamine and accompanied by a significant rise in serum concentration of immunoassayable gastrin. 15-Me-PGE2 caused a sudden and complete inhibition of gastric acid response to a peptone meal. 15-Me-PGE2 did not significantly affect serum gastrin levels both under basal conditions and in response to a peptone meal. Gastric acid and pepsin output induced by maximal stimulation with pentagastrin (4 mug/kg-hr) was inhibited by 15-Me-PGE2 by about 70% and that induced by histamine by about 45%. After the withdrawal of 15-Me-PGE2 infusion, gastric secretion remained reduced for the remainder of the test. We conclude that 15-Me-PGE2 is a very strong inhibitor of gastric acid and pepsin secretion induced by various secretory stimuli, particularly under basal conditions and in response to a meal. In view of prolonged inhibitory activity, 15-Me-PGE2 may have clinical potential in the treatment of peptic ulcer disease.