Ryan J R, Chremos A N, Vargas R, Mantell G, Johnson C L, McMahon F G
Clin Pharmacol Ther. 1987 Aug;42(2):225-31. doi: 10.1038/clpt.1987.136.
The antisecretory profile of the H2-receptor antagonist famotidine was studied with various oral doses and regimens in 10 healthy volunteers with high basal acid output (greater than or equal to 5 mEq/hr). Doses included 10, 20, and 40 mg at 9 PM and 9 AM and also 40 mg at 9 PM only. In the 22 hours after the PM doses, overnight (midnight to 7 AM) basal acid secretion was evaluated. Daytime meal-stimulated secretion was assessed at 7 AM, 12 noon, and 5 PM. Doses of 10, 20, and 40 mg inhibited fasting nocturnal basal secretion by 69%, 86%, and 83% to 94%, respectively (P less than 0.01). Meal-stimulated secretion at 7 AM (10 hours after administration) was inhibited by 28% and 39% (P less than 0.01) by only the 40 mg doses. The response to the 12 noon meal was inhibited by the 9 AM doses of 10, 20, and 40 mg by 45%, 75%, and 85%, respectively (P less than 0.01). The effect of a 40 mg dose given at 9 PM only had dissipated by breakfast (7 AM). The response to the 5 PM meal was suppressed by the 20 and 40 mg doses given at 9 AM by 22% and 35%, respectively (P less than 0.05). Suppression was present in only eight of the subjects after the 20 mg dose but in all 10 after the 40 mg dose. The effect on basal gastric aspirate pH values paralleled those seen on acid output. An association was found between mean plasma concentrations of famotidine and mean inhibition of meal-stimulated acid secretion. However, individual values may not be predictive.
