EFFECT OF SYNTHETIC PROSTAGLANDIN-E2 ANALOG ENPROSTIL ON OMEPRAZOLE-INDUCED HYPERGASTRINEMIA AND HYPERPEPSINOGENEMIA

This study was undertaken to determine whether the synthetic prostagla ndin E2 analog enprostil is able to inhibit basal and postprandial hyp ergastrinemia induced by omeprazole. We also studied the effect of ome prazole, enprostil and the combination of both drugs on serum pepsinog en A and C levels. Eight normal subjects received in random order five -day courses of 40 mg omeprazole once a day, 35 mug enprostil three ti mes a day, the combination of both drugs, and placebo. Omeprazole indu ced significant increases in basal and postprandial serum gastrin and in pepsinogen A and C levels. These increments persisted on the day af ter stopping treatment. Coadministration of enprostil inhibited omepra zole-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 signif icance for the postprandial integrated serum gastrin concentration. It is concluded that enprostil inhibits omeprazole-induced basal and pos tprandial hypergastrinemia, with a tendency to protracted inhibition a fter stopping the drugs, and that enprostil does not significantly inf luence omeprazole-induced increases in pepsinogen A and C level. Coadm inistration of enprostil may be helpful in preventing pronounced hyper gastrinemia in the few patients who show large serum gastrin increases during treatment with omeprazole.