EFFECT OF PLAUNOTOL ON HYPERGASTRINEMIA INDUCED BY LONG-TERM OMEPRAZOLE ADMINISTRATION IN HUMANS

Omeprazole markedly inhibits basal and stimulated gastric acid secreti on and has the ability to produce hypergastrinemia and hyperplasia of enterochromaffin-like cells in humans. On the other hand, paunotol, an acyclic diterpene alcohol, has been reported to inhibit gastrin relea se by stimulating endogenous secretin release. We investigated the eff ect of plaunotol on serum gastrin levels after six to eight weeks of o meprazole (20 mg/day) administration in 22 patients (16 males, 6 femal es; mean age 52.3, range 36-70 years) with peptic ulcer disease. The p atients were randomized to the following two groups: 11 subjects with omerprazole alone (single group) and 11 with omeprazole plus plaunotol (240 mg/day) (combination group) treatment. There were no significant differences between the two groups concerning age, sex, ulcer stage, ulcer history, environmental factors, and Helicobacter pylori (HP) pre valence. After complete drug(s) administration, serum immunoreactive ( ir) -gastrin levels increased significantly in the single group (P < 0 .001) in contrast to the combination group, and plaunotol significantl y inhibited hypergastrinemia induced by omeprazole administration (P < 0.001). Significant increases in serum ir-calcitonin gene-related pep tide concentrations were observed in the combination group compared to the single group (P < 0.05). However, there were no significant chang es in sereum ir-secretin, somatostatin, and vasoactive intestinal poly peptide levels as well as ulcer healing and HP prevalence between the two groups. These findings suggest that plaunotol may suppress hyperga strinemia induced by long-term omeprazole administration, at least par tly, via a certain brain-gut hormone affecting gastrin release.