Omepraole represents a new class of gastric acid secretion inhibitors. It is a clinically useful anti-ulcer agent of the pyridylmethyl-sulfinylbenzimidazole group which blocks the final common pathway of gastric acid secretion mainly by inhibiting proton pump in the parietal cells. In 15 endoscopically diagnosed duodenal ulcer patients, we measured the fasting serum gastrin and pepsinogen I levels, and ulcer healing status before and after a 20 mg omeprazole capsule per day for 14 days. Our results showed that fasting pepsinogen I level is significantly higher in duodenal ulcer patients, 99.21±8.76 and 63.48±488 ng/ml for duodenal ulcer and control groups respectively (p<0.001). With omeprazole treatment, fasting serum gastrin and pepsinogen I levels increased almost 2 folds from 35.92±3.57 to 68.92±9.10 pg/ml (p<0.01) and from 99.21±8.76 to 223.02±13.27 ng/ml (p<0.001) respectively. They all returned to pretreatment level (p>0.05) 2 weeks following drug discontinuation, which is associated with a high duodenal ulcer healing rate of 87%. In conclusion, the present study suggest that omeprazole not only a strong acid suppressor, which via inhibiting proton pump of parietal cells but also an inducer of hyperpepsinogenemia and hypergastrinemia, which may be due to direct or indirect or indirect effects on G cells and chief cells. The exact mechanism needs further investigation.
Omepraole represents a new class of gastric acid secretion inhibitors. It is a clinically useful anti-ulcer agent of the pyridylmethyl-sulfinylbenzimidazole group which blocks the final common pathway of gastric acid secretion mainly by inhibiting proton pump in the parietal cells. In 15 endoscopically diagnosed duodenal ulcer patients, we measured the fasting serum gastrin and pepsinogen I levels, and ulcer healing status before and after a 20 mg omeprazole capsule per day for 14 days. Our results showed that fasting pepsinogen I level is significantly higher in duodenal ulcer patients, 99.21±8.76 and 63.48±488 ng/ml for duodenal ulcer and control groups respectively (p<0.001). With omeprazole treatment, fasting serum gastrin and pepsinogen I levels increased almost 2 folds from 35.92±3.57 to 68.92±9.10 pg/ml (p<0.01) and from 99.21±8.76 to 223.02±13.27 ng/ml (p<0.001) respectively. They all returned to pretreatment level (p>0.05) 2 weeks following drug discontinuation, which is associated with a high duodenal ulcer healing rate of 87%. In conclusion, the present study suggest that omeprazole not only a strong acid suppressor, which via inhibiting proton pump of parietal cells but also an inducer of hyperpepsinogenemia and hypergastrinemia, which may be due to direct or indirect or indirect effects on G cells and chief cells. The exact mechanism needs further investigation.