Search

The role of omeprazole in preventing rebleeding in patients with peptic ulcer bleeding after successful endoscopic therapy has been controversial. In this study, we used 3 different formulas of intravenous omeprazole in the above patients. We wished to compare the intragastric pH and outcomes among them.Between July 1996 and May 1997, after having obtained initial hemostasis with endoscopic therapy, a total of 20 patients with peptic ulcer bleeding (spurting/oozing/non-bleeding visible vessel: 6/4/10) received intravenous bolus of omeprazole 20 mg every 3 hours; 20 patients (3/5/12) received intravenous bolus of omeprazole 40 mg every 6 hours; and, 20 patients (5/4/11) received intravenous bolus of omeprazole 80 mg every 12 hours for 3 days. One intragastric pH meter (Gastrograph Mark III, Medical Instruments Corp. Switzerland) was used to record 24-hour intragastic pH.The intragastric pH in the patients receiving omeprazole 20 mg every 3 hours was 6.1, 6.0-6.2 (mean: 95% CI); in patients receiving omeprazole 40 mg every 6 hours it was 6.4, 6.2-6.5; and, in patients receiving omeprazole 80 mg every 12 hours it was 5.8, 5.7-5.9. The duration of intragastric pH6.0 in omeprazole 20 mg every 3 hours was 70.9%, 57.3%-84.4% (mean: 95% CI); in omeprazole 40 mg every 6 hours it was 83.1%, 73.1%-93.1%; and, in omeprazole 80 mg every 12 hours it was 66%, 51.5%-80.4%. Patients with peptic ulcers receiving omeprazole 40 mg intravenous bolus every 6 hours had the highest intragastric pH as compared with the other 2 groups (p0.0001). There were no significant differences concerning rebleeding rates, volume of blood transfusion, hospital stay, numbers of operation and mortality among the 3 groups.After initial hemostasis had been obtained, patients with peptic ulcer bleeding receiving 40 mg intravenous bolus every 6 hours had the highest intragastric pH. However, they had similar outcomes with the other 2 groups.

Both Helicobacter pylori and non-steroidal anti-inflammatory drugs are reported to affect gastroduodenal prostaglandin synthesis. However, their influence on gastric mucosal prostaglandins remains unclear. The aim of this study was to investigate the influence of nonsteroidal anti-inflammatory drugs on mucosal prostaglandin synthesis in patients with Helicobacter pylori infection.We enrolled 87 Helicobacter pylori-infected patients in this study (gastric ulcer: 33, duodenal ulcer: 41, and non-ulcer dyspepsia: 13). Of them, 27 patients received non-steroidal anti-inflammatory drugs. Endoscopy was performed and biospy specimens from gastric body, antrum and duodenal bulb were assessed for Helicobacter pylori and prostaglandin concentration.A significantly lower mucosal prostaglandin E2 level at gastric body (142.2 +/- 28.1 ng/mg vs. 222.0 +/- 12.4 ng/mg, mean +/- SEM) and antrum (131.3 +/- 26.4 ng/mg vs. 226.0 +/- 19.0 ng/mg) was noted in Helicobacter pylori-infected gastric ulcer patients with non-steroidal anti-inflammatory drugs ingestion than in that of patients without non-steroidal anti-inflammatory drugs ingestion (p0.05). Using a multivariate analysis, we found that non-steroidal anti-inflammatory drug was an independent variable affecting gastric and duodenal mucosal prostaglandin E2 synthesis in patients with Helicobacter pylori-infected gastric ulcer.Non-steroidal anti-inflammatory drugs decrease gastroduodenal mucosal prostaglandin E2 synthesis in gastric ulcer patients with Helicobacter pylori infection.