Abstract
In recent years considerable progress has been made to elucidate the modes of action of colloidal bismuth subcitrate (CBS). CBS accelerates the healing of experimental chronic ulcers in rats by the formation of occlusive complexes and/or the accumulation of epidermal growth factor (EGF) in the ulcer crater. CBS exhibits gastric protection (cytoprotection) against, for example, ethanol lesions. Microscopic analysis of these lesions reveals that CBS protects against deep mucosal necrosis but not superficial injury, a property also found with prostaglandins. Dose-dependent increases in gastric prostaglandin E2 (PGE2) and bicarbonate secretion were found after CBS, in both animals and human volunteers. CBS in normal clinical doses increases PGE2 output from the gastric mucosa of human volunteers. Gastric injury in human volunteers produced by unbuffered aspirin is also reduced by concomitant administration of CBS, whereby PGE2 production is inhibited. This indicates that CBS exerts its gastric protection by both prostaglandin- and non-prostaglandin-mediated mechanisms. Campylobacter pylori is considered to be a causative factor of chronic antral gastritis and is a potential prerequisite for peptic ulcer disease. CBS, in contrast to other anti-ulcer drugs, prevents the growth of C. pylori in vitro. CBS eradicates C. pylori in patients and resolves chronic antral gastritis. The favourable relapse rates with CBS might be explained by the permanent eradication of C. pylori.
Published Version
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