No Helicobacter pylori, no Helicobacter pylori-associated peptic ulcer disease

Virtually all duodenal ulcers (DUs) and the vast majority of gastric ulcers (GUs) are the consequence of Helicobacter pylori-associated inflammation. In DUs, the inflammation is maximal in the antrum and is associated with gastric metaplasia in the bulb. Gastrin homeostasis is disturbed by H. pylori gastritis and there is robust acid secretion. Successful eradication of the infection cures the ulcer diathesis. Amalgamated figures for ulcer relapse per year in H. pylori-positive DUs are > 60% compared with 2.6% for H. pylori-negative DU patients. The corresponding figures for GU are > 50% for H. pylori-positive and 2.0% for H. pylori-negative individuals. This striking difference in relapse rate persists, as the re-infection rate in the developed world is < 1% per year. Recurrent bleeding in bleeding-prone DUs is essentially abolished after cure of the infection. Proton pump inhibitors (PPIs) are increasingly used in eradication regimens. PPIs have intrinsic antimicrobial activity. MICs for lansoprazole (LAN) are lower than for omeprazole (OME). Two weeks of triple therapy (bismuth, tetracycline, imidazole) has, on average, a superior eradication efficacy (> or = 90%) compared with dual therapy (PPI, amoxycillin or clarithromycin) (> or = 80%). When a combination of PPI and two antibiotics has been used, results comparable to triple therapy have been reported. However, the side-effects profile and patient acceptability of PPI plus one or two antibiotic regimens are better than for traditional triple therapy.(ABSTRACT TRUNCATED AT 250 WORDS)