Background: Antibiotic resistance of Helicobacter pylori is problematic because it reduces the efficacy of eradication therapy. It has been suggested that the incidence of resistance is rising. In Korea, information on the antimicrobial resistance of H. pylori is rare. The aim of this study was to assess the prevalence of H. pylori antibiotic resistance at a single center in Korea, and the changes in its antimicrobial resistance, and to detect the mutation foci of clarithromycin-resistant strains.
Methods: H. pylori isolates obtained from 224 patients with peptic ulcer disease in Korea between June 1996 and March 2000 were tested for antimicrobial resistance. The minimum inhibitory concentration (MIC) for metronidazole and clarithromycin was determined by the broth microdilution method. Isolates were considered resistant when the MIC was more than 8 microg/ml for metronidazole and more than 1 microg/ml for clarithromycin. To detect H. pylori 23S rRNA mutations, polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was performed. Sequencing was performed on the two strands of the nonrestricted amplicons.
Results: Overall, resistance to metronidazole and clarithromycin was detected in 41.9% and 5.4% of patients, respectively. There was no significant difference in metronidazole and clarithromycin resistance according to age group and sex. Six strains were resistant to both metronidazole and clarithromycin. Six of nine clarithromycin-resistant isolates possessed the A2144G mutation in the gene encoding 23S rRNA. Sequencing of the three non-restricted clarithromycin-resistant strains revealed a T-to-C mutation at position 2182.
Conclusions: In Korea, there was no significant increase in the prevalence of metronidazole resistance, but clarithromycin-resistant H. pylori strains had increased relatively over the 5-year period. There was an increasing tendency for the emergence of strains with dual resistance to metronidazole and clarithromycin. Many of the clarithromycin-resistant strains possessed the A2144G mutation.