Types of 23S Ribosomal RNA Point Mutations and Therapeutic Outcomes for Helicobacter pylori

Abstract

Background/Aims Point mutations in the 23S ribosomal RNA gene have been associated with Helicobacter pylori clarithromycin resistance. This study aimed to detect the prevalence of these point mutations and to investigate the role of different point mutations in the success of eradication therapy. Methods We retrospectively investigated a total of 464 consecutive patients who underwent an endoscopic examination and dual-priming oligonucleotide-based multiplex polymerase chain reaction for H. pylori between June 2014 and October 2019. For 289 patients with negative point mutations, standard triple therapy was used in 287 patients, and the bismuth-quadruple regimen was used in two patients. For 175 patients with positive point mutations (A2142G, A2143G, and both mutations), standard triple and bismuth-quadruple therapies were used in 37 patients and 138 patients, respectively. Results The eradication rates of standard triple and bismuth-quadruple therapies showed no significant difference in mutation-negative patients or those with the A2142G point mutation. However, the eradication rate with bismuth-quadruple therapy was significantly higher than that with standard triple therapy in the group with the A2143G mutation or with the double mutation. The eradication rates for standard triple and bismuth-quadruple therapies, respectively, were 25.8% and 92.1% in the per-protocol group (p<0.001) and 24.2% and 85.2% in the intention-to-treat analysis (p<0.001). Conclusions The A2143G point mutation is the most prevalent cause of clarithromycin resistance. Bismuth-quadruple therapy is superior to standard triple therapy in patients with the A2143G or double point mutation.

Characteristics of Helicobacter pylori Heteroresistance in Gastric Biopsies and Its Clinical Relevance

“…Antimicrobial resistance has been thought to be the main reason for this situation. The eradication rate with bismuth-quadruple therapy was significantly higher than that with standard triple therapy in the group with the A2143G mutation or with the double mutation (Kim et al, 2021). In Europe, the resistance rate for CLA and LEV was approximately 21.4% and 15.8%, respectively (Megraud et al, 2021).…”

“…Besides, bacteria resistance to the antibiotic may also be varied. For example, a resistance genotype of CLA could be mutated as A2142C/G or A2143G in 23S rRNA gene, and resistance genotype of LEV could be mutated in the 87th amino acid and/or 91st amino acid (Wang et al, 2020;Domanovich-Asor et al, 2021;Kim et al, 2021). Does heteroresistance for these antibiotics show different characteristics?…”

Current guidelines for Helicobacter pylori treatment in East Asia 2022: Differences among China, Japan, and South Korea

“…As an alternative, molecular methods for detecting CAM resistance are available for tailored H. pylori eradication in South Korea[ 60 ]. H. pylori resistance against CAM is mediated by point mutations in 23S ribosomal RNA[ 61 ]. The treatment regimen is selected based on the presence of the A2142G and A2143G point mutations that cause CAM resistance[ 62 ].…”

Benefits of a Molecular-Based Method for the Detection of Clarithromycin-Resistant Helicobacter pylori

“…In this issue of Gut and Liver, Kim et al 4 examined the prevalence of resistance to clarithromycin related to point mutations using a dual-priming oligonucleotide (DPO)based multiplex polymerase chain reaction (PCR) assay and assessed the impact of different point mutations on the success of eradication therapy. This retrospective cohort study examined 464 patients by reviewing databases in Korea between June 2014 and October 2019.…”

“…In summary, Kim et al 4 studied how application of the DPO-based multiplex PCR assay in clinical practice to detect clarithromycin-resistant cases, may improve the cure rate of H. pylori infection. Future studies focused on tailored therapy should aim to reduce the incidence of resistance in H. pylori infections, apply this to clinical practice, and develop strategies that depend on population-specific resistance mechanisms.…”