Drug Resistance in Helicobacter pylori

Initial studies have suggested that eradication of Helicobacter pylori is associated with lower duodenal ulcer relapse rates [1, 2]. Hence there has been continued effort in identifying the optimum antibacterial regimen for total clearance of H. pylori. Even before the discovery of the association of H. pylori with gastroduodenal disease, bismuth had been used successfully in the treatment of duodenal ulcers [3]. It was thought that this effect was achieved merely by mucosal protection as the drug binds to gastric mucin producing a complex which adheres to the ulcer crater and retards hydrogen ion diffusion. H2-receptor antagonists were introduced in the 1970s and were found to be equally as effective as bismuth in the immediate healing of duodenal ulcers. However, there was a significant difference in the ulcer relapse rates. Of duodenal ulcers 60 %–90 % relapsed within 1 year when treated with H2-receptor antagonists but only 35%–76% of duodenal ulcers treated with bismuth relapsed during this time. Bismuth was also found to be better than H2-receptor antagonists in healing the associated antral gastritis [4, 5]. Bismuth has since then been widely used in the treatment of duodenal ulcer.