Antimicrobial resistance in Helicobacter pylori

Helicobacter pylori is associated with chronic gastritis, peptic ulcer dise ase, gastric carcinoma and gastric lymphoma. Triple treatment consisting of a proton pump inhibitor and two antibiotics out of amoxycillin, clarithrom ycin and metronidazole is the eradication therapy of choice. The clinical r elevance of H. pylori resistance is still controversial, but resistance is generally assumed to be a major obstacle to effective eradication of this m icroorganism - in particular resistance to clarithromycin and, to a lesser extent, metronidazole. Clarithromycin resistance is caused by point mutatio ns in the peptidyl transferase domain of the 23S rRNA ribosomal subunit whe reas metronidazole resistance generally involves mutational inactivation of the rdxA gene, which encodes a NADPH nitroreductase that reduces nitroimid azole to active metabolites. Resistance to both antibiotics may vary betwee n countries and populations. In Europe, clarithromycin resistance has reach ed 12-15% in the Mediterranean area whereas in northern countries it is les s than 3%. Metronidazole resistance is higher in developing than in develop ed countries, reaching 80-90% in Africa. Tetracycline resistance is still r are and the resistance mechanism has not yet been characterised. Amoxycilli n resistance in H. pylori is an emerging problem. Resistant strains are tol erant to this antibiotic and show modification in the penicillin-binding pr otein profile. Most resistance in H. pylori occurs by mutation and resistan t strains may be selected under inappropriate antimicrobial pressure. Knowl edge of the susceptibility profile of H. pylori would allow the selection o f adequate antimicrobial treatment. (C) 2001 Lippincott Williams & Wilkins.