Effect of synthetic prostaglandin E2 analog enprostil on omeprazole-induced hypergastrinemia and hyperpepsinogenemia

• Published in: Digestive diseases and sciences Vol. 39; no. 3; pp. 609 - 616
• Main Authors: MEIJER, J. L, CROBACH, L. F. S. J, JANSEN, J. B. M. J, LAMERS, C. B. H. W
• Format: Journal Article
• Language: English
• Published: Heidelberg Springer 01-03-1994
• Subjects: Adult; Biological and medical sciences; Digestive system; Drug Therapy, Combination; Enprostil - administration & dosage; Enprostil - adverse effects; Enprostil - pharmacology; Female; Gastrins - blood; Humans; Male; Medical sciences; Omeprazole - administration & dosage; Omeprazole - adverse effects; Omeprazole - pharmacology; Pepsinogens - blood; Pharmacology. Drug treatments; Human; Peptide hormone; Prostaglandin E2; Biological activity; Hypergastrinemia; Chemotherapy; Gastrointestinal hormone; Treatment; Analog; Antisecretory agent; Gastrin; Combined treatment; Prostaglandin derivatives
• ISSN: 0163-2116; 1573-2568
• DOI: 10.1007/BF02088350

This study was undertaken to determine whether the synthetic prostaglandin E2 analog enprostil is able to inhibit basal and postprandial hypergastrinemia induced by omeprazole. We also studied the effect of omeprazole, enprostil, and the combination of both drugs on serum pepsinogen A and C levels. Eight normal subjects received in random order five-day courses of 40 mg omeprazole once a day, 35 micrograms enprostil three times a day, the combination of both drugs, and placebo. Omeprazole induced significant increases in basal and postprandial serum gastrin and in pepsinogen A and C levels. These increments persisted on the day after stopping treatment. Coadministration of enprostil inhibited omeprazole-induced basal hypergastrinemia and postprandial integrated serum gastrin, but not basal serum pepsinogen A and C, while the inhibition on the day after the treatment courses only reached statistical significance for the postprandial integrated serum gastrin concentration. It is concluded that enprostil inhibits omeprazole-induced basal and postprandial hypergastrinemia, with a tendency to protracted inhibition after stopping the drugs, and that enprostil does not significantly influence omeprazole-induced increases in pepsinogen A and C level. Coadministration of enprostil may be helpful in preventing pronounced hypergastrinemia in the few patients who show large serum gastrin increases during treatment with omeprazole.