Rapid protection of the gastroduodenal mucosa against aspirin-induced damage by rabeprazole.

BACKGROUND: The ability of a proton pump inhibitor to reduce or prevent NSAID-induced gastroduodenal damage during the first 24 h has not been tested. AIM: To determine, whether oral rabeprazole, administered 5 h before the initiation of therapeutic dosing of aspirin protects the gastroduodenal mucosa. METHODS: Normal subjects were randomized into two groups - one received rabeprazole, 20 mg at 07:00 hours and the other placebo, before initiation of aspirin 650 mg at 12:00 hours, and then q4 h for 3 days. Upper endoscopic examinations were performed on all subjects at baseline, 24 and 72 h after initiation of aspirin. Gastroduodenal mucosal damage was scored. RESULTS: Thirty subjects were compliant with study medications and underwent three endoscopic examinations. Salicylate concentrations were similar for the placebo and the rabeprazole groups at all times. On rabeprazole, the Lanza scores were significantly lower compared with placebo at 24 h (1.3 +/- 0.26 vs. 2.1 +/- 0.26, P < 0.05) and at 72 h (1.3 +/- 0.29 vs. 2.3 +/- 0.28, P < 0.05). Gastric antral erosion counts were less with rabeprazole than placebo at 24 (4.1 +/- 1.3 vs. 7.6 +/- 2.0, P > 0.05) and 72 h (5.3 +/- 1.8 vs. 8.0 +/- 1.5; P > 0.05). CONCLUSIONS: Rabeprazole, initiated 5 h before the start of therapeutic dosing with aspirin, decreased Lanza scores and antral erosion counts at 24 h. These findings suggest that prophylaxis with rabeprazole could start concurrently with aspirin administration.

High-resolution solid-state manometry of the antropyloroduodenal region.

Manometric recording from the pyloric channel is challenging and is usually performed with a sleeve device. Recently, a solid-state manometry system was developed, which incorporates 36 circumferential pressure sensors spaced at 1-cm intervals. Our aim was to use this system to determine whether it provided useful manometric measurements of the pyloric region. We recruited 10 healthy subjects (7 males:3 females). The catheter (ManoScan(360)) was introduced transnasally and, in the final position, 15-20 sensors were in the stomach and the remainder distributed across the pylorus and duodenum. Patients were recorded fasting and then given a meal and recorded postprandially. Using pressure data and isocontour plots, the pylorus was identified in all subjects. Mean pyloric width was 2.1 +/- 0.1 cm (95% CI: 1.40-2.40). Basal pyloric pressure during phase I was 9.4 +/- 1.1 mmHg, while basal antral pressure was significantly lower (P = 0.003; 95% CI: 2.4-8.4). Pyloric pressure was always elevated relative to antral pressure in phase I. For phases II and III, pyloric pressure was 7.7 +/- 2.3 mmHg and 9.4 +/- 1.1 mmHg, respectively. Pyloric pressure increased similarly after both the liquid and solid meal. In addition, isolated pressure events and waves, which involve the pylorus, were readily identified.