METHODS: H. pylori-positive patients were assigned to Group A (7-day STT; rabeprazole 20 mg twice daily, amoxicillin 1 g twice daily, and clarithromycin 500 mg twice daily, for 7 days), Group B (7-day STT with bismuth; rabeprazole 20 mg twice daily, amoxicillin 1 g twice daily, clarithromycin 500 mg twice daily and bismuth subcitrate 240 mg twice daily, for 7 days) and Group C (14-day STT; rabeprazole 20 mg twice daily, amoxicillin 1 g twice daily, and clarithromycin 500 mg twice daily for 14 days). Eradication was tested using 13 C-UBT at least 4 weeks after the completion of therapy.
RESULTS: A total of 364 patients were recruited. In the intention-to-treat analysis, eradication rates were 79.3% (96/121; 95% confidence interval [CI] 71.3-85.6%) for 7-day STT, 81.7% (98/120; 95% CI 73.8-87.6%) for 7-day STT with bismuth, and 88.6% (109/123; 95% CI 81.8-93.1%) for 14-day STT, respectively. Statistical significance was achieved between the 7-day and the 14-day STT treatment (P = 0.048).
CONCLUSIONS: Adding bismuth to the 7-day STT did not result in an increase in the eradication rate. Extending the STT to 14 days, however, achieved a significantly higher eradication rate. Nevertheless, this did not achieve the targeted 90% eradication rate on intention-to-treat analysis.
Methods: Here, we investigated the impact of the CYP2C19 genotype polymorphism and the success of triple therapy (fluoroquinolones/metronidazole/clarithromycin) on antibiotic-resistant strains in eradicating H. pylori in human subjects with non-ulcer dyspepsia (NUD), in human subjects with peptic ulcer disease (PUD) and in asymptomatic human subjects (positive and negative for H. pylori infection).
Results: Based on the CYP2C19 genotypes, determined by Droplet Digital PCR (ddPCR) analysis, we found 11.2%, 62.5% and 26.3% corresponding to rapid metabolizers, intermediate metabolizers and poor metabolizers, respectively. However, we did not find any significant effect for homozygous ABCB1 or CYP2C19*2 and CYP2C19*3 alleles. We detected several participants heterozygous for both ABCB1 and CYP2C19*2, CYP2C19*3 and CYP2C19*17 loci. The participants heterozygous for both ABCB1 and CYP2C19*2 and *3 loci should be defined as intermediate and poor metabolizers according to the haplotype analysis in the NUD, PUD and asymptomatic subjects.
Conclusions: Consequently, fluoroquinolones/metronidazole/clarithromycin-based triple therapies can be used to eradicate H. pylori infection, if one does not know the CYP2C19 genotype of the patient.
RESULTS: The S isolates with A2143G mutation in the 23S rRNA gene were successfully induced to be resistant. According to the data, antibiotic exposure may alter the expression of certain genes, including those that code for the Cag4/Cag protein, the vacuolating cytotoxin domain-containing protein, the sel1 repeat family protein, and the rsmh gene, which may increase the risk of developing and enhances virulence in H. pylori. Enhanced biofilm formation was detected among R isolates compared to B and S isolates. Furthermore, high polymorphism was also detected among the genes associated with biofilm production.
CONCLUSIONS: Therefore, this study suggests that H. pylori may acquire virulence factors while also developing antibiotic resistance due to clarithromycin exposure.