HELICOBACTER PYLORI

Peptic ulcer disease caused by H. pylori infection is treated by associations of antibiotics, which may include amoxicillin, tetracyclines, clarithromycin and metronidazole. Eradication fails, however, in 10–30% of cases. This is in part due to primary or secondary resistance to one or more of these drugs, most commonly to metronidazole or clarithromycin. Development of secondary resistance may occur in over 50% of cases with suboptimal regimens. Nitroimidazole resistance is mostly related to mutational inactivation of the rdxA gene encoding an oxygen-sensitive NADPH nitroreductase. The cure rate with most combination regimens drops by about 50% in case of nitroimidazole resistance. The prevalence of this resistance is rising and currently ranges from 10% to 40% of isolates in the West and from 50% to 80% in developing countries. Resistance to clarithromycin is caused by a mutation at position 2142 or 2143 in 23S rRNA. Its impact on cure rate appears similar to that of nitroimidazole resistance for most treatment regimens. The prevalence of primary macrolide resistance varies by region between 3% and 25% and is increasing. Standardization of resistance detection methods for this pathogen is much needed to assess the efficacy of treatment regimens based on primary resistance patterns and to guide local recommendations based on surveillance data.
The prevalence of resistance to amoxicillin and to tetracycline is very low (<1%) in H. pylori except in a few countries like South Korea. In contrast, resistance to fluoroquinolones, mainly caused by mutation in the gyrA gene, shows a higher prevalence (9–20%).