Mifentidine is a new H2-receptor antagonist with distinct characteristics of potency and long plasma half-life. The aim of this study was to evaluate the effects of
mifentidine on
peptone meal-stimulated gastric acid secretion. Nine
duodenal ulcer patients in remission were enrolled in the study and given in double-blind and at random, on two different occasions, a single
tablet of 10 or 20 mg
mifentidine or placebo according to an incomplete balanced block design. Ninety min after ingestion of the
drug, basal gastric secretion was collected for 30 min and volume, pH and
acid output determined. Thereafter, the
acid output following
peptone meal-stimulation was measured for 2 h by a modified version of the intragastric titration method of Thompson and Swierczek. Plasma samples were collected for
gastrin and
mifentidine determinations. Basal
acid output was strongly inhibited by both the low dose (-78%) and the high dose (-98%) (p less than 0.01). The
peptone meal-stimulated
acid output was reduced in a dose-dependent manner (-45% by 10 mg and -90% by 20 mg). The
drug did not affect the fasting serum
gastrin levels but increased, although not significantly, the
gastrin response to food. The log of the area under the
mifentidine plasma levels correlated linearly with total
acid output (p less than 0.01). The results of this study indicate that
mifentidine dose-dependently suppresses basal
acid secretion and reduces
peptone-stimulated gastric acid secretion in
duodenal ulcer patients.