Azam Shareh , Behnoush Khasheii , Tayebeh Faraji , Masoud Khoshnia , Shaghayegh Anvari , Ailar Jamalli ,
Volume 19, Issue 4 (Jul-Aug 2025)
Abstract
Background: Antibiotic resistance in Helicobacter pylori infections can lead to treatment failure. This study aims to evaluate the antibiotic resistance to metronidazole, clarithromycin, and fluoroquinolone in H. pylori strains isolated from gastric biopsy specimens.
Methods: This study was conducted between 2016 and 2017 on 80 biopsy specimens obtained from Golestan province. Resistance to metronidazole (rdxA) and fluoroquinolones (gyrA) was determined using PCR. Mutations in the loci of the 23S rRNA gene associated with clarithromycin resistance were analyzed using PCR-RFLP with the BsaI and BbsI enzymes.
Results: In this study, 25% of H. pylori strains showed resistance to clarithromycin. Mutations in the A2143G locus (65%) and the A2142G locus (35%) were detected in these strains. Resistance to fluoroquinolones (27.5%) was observed, with the most common mutations being at the 91 amino acid position of aspartate (63.63%) and the 87 amino acid position of asparagine (36.36%). Resistance to metronidazole was not observed in any of the strains of this study, and concomitant resistance to clarithromycin and fluoroquinolones was observed in 13.75% of H. pylori strains.
Conclusion: According to our study, in Iran, the resistance of H. pylori to clarithromycin is increasing, which may lead to treatment failure. The mechanism of clarithromycin resistance is related to mutations in the A2143G and A2142G positions, and a mutation in the gyrA gene causes resistance to fluoroquinolones, which often occurs in the 91 amino acid position.