Molecular detection of genotypic clarithromycin‐resistant strains and its effect on the eradication rate of concomitant therapy in Helicobacter pylori infection

Abstract

Antimicrobial eradication rates for Helicobacter pylori have been decreasing and the reason for treatment failure was found to be resistance to one or more of the antibiotics. Clarithromycin resistance to H pylori was associated with point mutations in the 23S rRNA gene and the PCR-RFLP method can detect these point mutations. The aim of this study was to determine the molecular detection of genotypic clarithromycin-resistant strains and its effect on the eradication rate of concomitant therapy in H pylori infection. The presence of H pylori DNA was confirmed by amplifying the UreC gene by polymerase chain reaction (PCR) and point mutations on 23S rRNA (A2142G and A2143G) were detected by PCR-RFLP. A total of 98 H pylori-infected patients were involved and among them, genotypic clarithromycin-sensitive strain was 93.9% and clarithromycin-resistant strain was 6.1%. All patients were found to have the A2143G point mutation but A2142G was not detected. Successful eradication rate of concomitant therapy was found to be 89.8% and unsuccessful rate was 10.2%. Among patients with the clarithromycin-resistant gene, only 16.7% had successful eradication and 83.3% had unsuccessful eradication. There was a statistically significant association between failure rate of concomitant therapy and detection of clarithromycin-resistant genes (P < 0.01). The presence of A2143G point mutation in the clarithromycin-resistant strain has a negative effect on the eradication rate of H pylori infection.