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Resistance of Helicobacter pylori to quinolones and clarithromycin assessed by genetic testing in Japan
Author(s) -
Yamade Mihoko,
Sugimoto Mitsushige,
Uotani Takahiro,
Nishino Masafumi,
Kodaira Chise,
Furuta Takahisa
Publication year - 2011
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/j.1440-1746.2011.06815.x
Subject(s) - clarithromycin , helicobacter pylori , medicine , quinolone , amoxicillin , antibiotics , 23s ribosomal rna , gastroenterology , incidence (geometry) , microbiology and biotechnology , antibacterial agent , biology , gene , physics , optics , ribosome , rna , biochemistry
Background and Aim: As bacterial resistance to clarithromycin limits the efficacy of clarithromycin‐based regimens for Helicobacter pylori infection, attention has turned to quinolone‐based rescue therapies. Resistance of H. pylori to both clarithromycin and quinolone can be predicted by genetic testing. Here, we used this approach to evaluate the prevalence of clarithromycin‐ and quinolone‐resistant strains of H. pylori in Japan. Methods: DNA was extracted from gastric tissue samples obtained from 153 patients infected with H. pylori (103 naive for eradication therapy and 50 with previous eradication failure following triple proton pump inhibitor/amoxicillin/clarithromycin therapy). Mutations in H. pylori 23S rRNA and gyrA genes associated with resistance to clarithromycin and quinolones, respectively, were determined. Results: Of 153 patients, 85 (55.6%) were infected with clarithromycin‐resistant strains. The prevalence of clarithromycin‐resistant strains in patients with previous eradication failure (90.0%, 45/50) was significantly higher than that (38.8%, 40/103) of those naive for eradication therapy ( P < 0.001). Fifty‐nine patients (38.6%) were infected with strains resistant to quinolones. The incidence of quinolone‐resistant strains also appeared higher in patients with eradication failure (48.0%, 24/50) than in those who had not undergone therapy (34.0%, 35/103); however, the difference was not statistically significant ( P = 0.112). The incidence of quinolone‐resistance in clarithromycin‐resistant strains (44/85, 51.8%) was significantly higher than that in clarithromycin‐sensitive strains (15/68, 22.1%) ( P < 0.001). Conclusions: A high incidence of quinolone‐resistance was found in clarithromycin‐resistant strains of H. pylori , particularly in patients with previous eradication failure. Our results suggest that testing for susceptibility of H. pylori to quinolones is useful for determining the optimal rescue eradication regimen.