High concentrations of bile acid seem to be associated with an elevated risk of intestinal metaplasia.

SUMMARYBackground: Several studies in Western countries showed that proton-pump inhibitors are superior to histamine 2 -receptor antagonists or placebo in the treatment of non-erosive gastro-oesophageal reflux disease. The efficacy of acid-suppressive drugs for nonerosive gastro-oesophageal reflux disease in Japan, in which the prevalence of Helicobacter pylori infection is higher compared with Western countries, is unknown. Aim: To compare the efficacy of famotidine and omeprazole in Japanese patients with non-erosive gastro-oesophageal reflux disease by a prospective randomized multicentre trial. Methods: A total of 98 patients received either famotidine 20 mg b.d. (n ¼ 48) or omeprazole once daily (n ¼ 50). Frequency of gastro-oesophageal reflux disease symptoms and health-related quality of life were evaluated at baseline and after 4 weeks of treatment.

Improving the quality of ulcer healing (QOUH) is one of the valid methods of prevention of relapse of gastric ulcers. We investigated the effect of lafutidine on the QOUH of gastric ulcer compared with famotidine in a randomized, multi-centre controlled trial. Consecutive 80 patients with a gastric ulcer were randomly assigned to receive twice daily either lafutidine (10 mg) or famotidine (20 mg) for 12 weeks. Esophagogastroduodenoscopy was performed to examine the ulcer healing rate and rate of flat type ulcer scars using dye-contrast. The gastric ulcer healing rate was 92.1% in the lafutidine group (35/38) and 94.7% in the famotidine group (36/38). The rate of flat-type ulcer scars was significantly higher in the lafutidine group (68.4%, 26/38) than in the famotidine group (42.1%, 16/38) (P = 0.021). In conclusion, the present study demonstrated that lafutidine, as compared to famotidine, yields a significantly superior QOUH in patients with gastric ulcers in the clinical setting.

We investigated the effect of stress on the prostaglandin E2 levels in rat gastric mucosa. In untreated controls, prostaglandin E2 levels were higher in the antral than the fundic mucosa. Stress experiments showed tht 30-min stress induced no gastric lesions but effected a significant (p less than 0.05) increase in antral prostaglandin E2: after 7-hr stress exposure, hemorrhagic lesions and prostaglandin E2 levels significantly (p less than 0.05) below normal control values were noted. The formation of HCl-induced gastric mucosal lesions was markedly inhibited if 30-min stress preceded HCl-administration. The infusion of 5 microgram/kg 16, 16-dimethyl prostaglandin E2 prior to 7-hr stress exposure inhibited ulcer formation markedly. Our results suggested that stress-induced decrease in intramucosal prostaglandin E2 plays an important role in the pathogenesis of stress ulcer formation.

The effects of 16,16-dimethyl prostaglandin E2 PGE2 on gastric mucosal blood flow and gastric mucosal damage were tested in rats given indomethacin. Blood flow was measured by hydrogen gas clearance. Indomethacin given intragastrically reduced the blood flow in nonlesion areas and the levels of PGE2 and 6-keto-PGF1 alpha in the gastric mucosa and caused mucosal damage in a dose-related way. Indomethacin (20 mg/kg) significantly reduced the blood flow 30 min after administration, and the reduction increased until 90 min. Then the flow plateaued until 240 min. Gastric mucosal damage caused by 20 mg/kg of indomethacin and evaluated by only gross observations, began at 60 min and developed with time until 240 min after administration. 16,16-Dimethyl PGE2 (5 micrograms/kg) did not affect the reduction of blood flow caused by indomethacin during 240 min of measurements, but it significantly inhibited the indomethacin-induced mucosal damage evaluated by gross observations. These results suggest that prevention by 16,16-dimethyl PGE2 of grossly observed gastric mucosal damage caused by indomethacin was not related by preservation of the gastric mucosal blood flow in the areas without lesions.