Extensive clinical studies of Helicobacter pylori have shown this bacterium to be an important causative factor of peptic ulcer, particularly in its recurrence. Therefore, numerous therapeutic trials for the eradication of H. pylori have been reported. A recent trend in curative therapy has been so-called triple therapy, using a proton pump inhibitor and two different antimicrobials. 1 Sucralfate, which is a widely used cytoprotective agent for the gastric mucosa, is reported to inhibit several of the activities of H. pylori and to enhance the anti-H. pylori activity of antimicrobial agents. 2±11 Therefore, several studies of sucralfate-based eradication therapy have been reported recently. 12±18 However, the ef®cacy and safety of sucralfate-based therapy are still controversial. 19±20 The present study was designed to evaluate the ef®cacy and safety of sucralfate in combination with amoxycillin and clarithromycin as eradication therapy for H. pylori, in comparison with lansoprazole-based triple therapy. PATIENTS AND METHODS PatientsThis study was designed as a prospective, randomized, multicentre study, and was carried out in accordance SUMMARY Background: Sucralfate has an inhibitory action against Helicobacter pylori and enhances the anti-H. pylori activity of antimicrobials. Aim: To evaluate the ef®cacy and safety of sucralfatebased eradication therapy for H. pylori infection, compared with that based on lansoprazole, in a randomized multicentre study. Subjects and methods: The subjects were 150 H. pyloripositive patients. They were randomly assigned to one of two regimens for 2 weeks: sucralfate 1 g t.d.s., amoxycillin 500 mg t.

Background: S‐0509, 2‐[(tert‐butoxycarbonylmethyl) [(m‐(carboxy‐phenyl)‐ureidomethyl‐carbonyl]] aminobenzo phenone, was developed as a potent and selective CCKB/gastrin receptor antagonist that does not affect the central nervous system. Methods: We evaluated the effects of S‐0509 on gastric acid secretion and duodenal ulcerogenic and healing responses in rats comparing it with L‐365,260, another CCKB/gastrin receptor antagonist. Results: S‐0509 (0.1~10 mg/kg, i.d.) was able to dose‐dependently decrease basal acid secretion and inhibit the acid secretory responses induced by both pentagastrin (60 μg/kg/h, i.v.) and peptone (10%, i.g.) but not histamine (4 mg/kg/hr, i.v.) or carbachol (60 μg/kg/h, i.v.). L‐365,260 (10 and 30 mg/kg, i.d.) caused only partial a suppression of the acid secretory response to pentagastrin but not to other stimuli, including peptone treatment. On the other hand, a duodenal ulcerogen, mepirizole (200 mg/kg, s.c.) caused an increase in acid secretion and resulted in penetrating ulcers in the proximal duodenum, and these ulcers gradually healed over 3 weeks. S‐0509 significantly inhibited both the acid secretory (> 1.0 mg/kg, i.d.) and ulcerogenic (> 3 mg/kg, p.o.) responses induced by mepirizole when it was given as a pre‐treatment. It also promoted significantly the healing of these ulcers (> 3 × 2 mg/kg, p.o.) when it was given twice daily for 14 days. In contrast, L‐365,260 (30 mg/kg) tended to reduce the severity of mepirizole‐induced duodenal ulcers, with a slight inhibition of acid secretion, but it caused no influence on the healing response of these ulcers. Conclusion: These results confirmed that S‐0509 is a selective CCKB/gastrin receptor antagonist with potent antisecretory action in vivo conditions, and further demonstrated that this agent not only prevents the development of duodenal ulcers but also shows healing promoting action on duodenal ulcers, probably through the blockade of CCKB/gastrin receptors.

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