Heterogeneity of Helicobacter pylori Strains Isolated from Patients with Gastric Disorders in Guiyang, China

Mi, Mengheng; Wu, Fang; Zhu, Jian; Liu, Fang; Cui, Guizhong; Wen, Xueqing; Hu, Yue; Deng, Zhongwei; Wu, Xiaojuan; Zhang, Zhengrong; Qi, Ting-Na; Chen, Zhenghong

doi:10.2147/idr.s287631

Cited by 11 publications

(15 citation statements)

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“…Some authors have analyzed the virulence genes and clarithromycin resistance, and it has been suggested that H. pylori vacA and cagA genotypes affect the eradication rates of bacteria [ 55 , 56 ]. Our study reported that the vacA s1m1/cagA + genotype was associated with the A2142G mutation.…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori Virulence Factors and Clarithromycin Resistance-Associated Mutations in Mexican Patients

et al. 2023

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Persistent infection with Helicobacter pylori (H. pylori) is an important factor in gastric diseases. The vacA and cagA virulence factors of H. pylori contribute to the development of these diseases. Triple therapy containing clarithromycin has been used to eradicate this infection. Unfortunately, resistance to this antibiotic is the primary cause of treatment failure. This study aimed to determine the prevalence of clarithromycin resistance-associated mutations and to assess the relationship between virulence factors and Mexican patients infected with H. pylori. The cagA and vacA genotypes were determined by multiplex PCR. Furthermore, a qPCR was used to identify mutations of the 23S rRNA gene. This study reported a prevalence of 84.3% of H. pylori among patients with gastric diseases, and the vacA s1m1/cagA+ genotype was the most frequent (44.8%) in antrum and corpus. Analysis of the 23S rRNA gene revealed a 19.8% prevalence of clarithromycin resistance-associated mutations. The most prevalent mutations were A2143G (56%) and A2142C (25%). A significant association (p < 0.05) between the A2142G and the vacA s1m1/cagA+ genotype was detected. In conclusion, we report a high prevalence (>15%) of clarithromycin resistance-associated mutations, and we found an association between the genotypes of virulence factors and a mutation in the 23S rRNA gene.

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Section: Discussionmentioning

confidence: 99%

Helicobacter pylori Virulence Factors and Clarithromycin Resistance-Associated Mutations in Mexican Patients

et al. 2023

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“…There is a possibility that other clinically significant point mutations exist, such as A2142C, A2143C, and A2144G, that are not currently detected by DPO-PCR, 21 although these mutations alone are associated with less than 5% of clarithromycin-resistant H. pylori isolates in Korea. 21,27 Due to the common heterogeneity of H. pylori, even within one individual, 28 the tissue biopsy-based DPO-PCR has the inherent potential bias of false-negative results, which may contribute to treatment failures. In addition, different individual CYP2C9 polymorphism that affects the proton pump inhibitor metabolism can be considered another cause.…”

Section: Discussionmentioning

confidence: 99%

Effective Eradication Regimen and Duration According to the Clarithromycin Susceptibility of Helicobacter pylori Determined Using Dual Priming Oligonucleotide-Based Multiplex Polymerase Chain Reaction

Kim

et al. 2022

Gut and Liver

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Background/Aims: Dual priming oligonucleotide-based multiplex polymerase chain reaction (DPO-PCR) has recently been used for both the detection of Helicobacter pylori and the identification of H. pylori 23S ribosomal RNA point mutations that cause clarithromycin resistance. The aim of this study was to investigate the duration of effective standard triple therapy in a clarithromycin susceptible group and of bismuth-based quadruple therapy in a resistant group based on DPO-PCR. Methods:We retrospectively analyzed the electronic medical records of 184 patients who, between September 2019 and December 2020, received eradication therapy following detection of H. pylori, and the subsequent identification of the clarithromycin susceptibility of their H. pylori using DPO-PCR. Patients were treated with 7-or 14-day standard triple therapy in the clarithromycin susceptible group, whereas 7-or 14-day bismuth-based quadruple therapy in the clarithromycin resistance group. Results:In the clarithromycin susceptible group, per-protocol analyses showed eradication rates of 87.5% (42/48; 95% confidence interval [CI], 77.1% to 95.8%) for 7-day therapy and 87.2% (41/47; 95% CI, 78.7 to 95.7%) for 14-day therapy (p=0.969). The eradication rates in the clarithromycin resistance group were 91.4% (32/35; 95% CI, 80.0% to 100.0%) for 7-day therapy and 90.3% (28/31; 95% CI, 77.4% to 100.0%) for 14-day therapy (p=0.876). There was no significant difference in the eradication rates, patient compliance, or rate of adverse events between the 7-and 14-day therapies for both groups.Conclusions: Compared to the 14-day therapy, 7-day eradication therapy is sufficient after DPO-PCR-based clarithromycin susceptibility testing.

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“…Such genetic variability proves drug susceptibility therapy difficult and poses the danger of the evolution of more virulent and adapted strains. In the study of Mi et al [ 88 ] using cagA typing and RAPD-PCR fingerprinting, H. pylori strain isolated from patients showed heterogenicity that were considered to indicate the incidence of multiple infections. Overall, the different clinical outcomes during H. pylori infection may be due to differences in H. pylori strains—this could act as a marker to predict H. pylori disease outcomes [ 89 ].…”

Section: An Overview Of H Pylori Infectionmentioning

confidence: 99%

Helicobacter pylori: an up-to-date overview on the virulence and pathogenesis mechanisms

2022

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Helicobacter pylori is an organism associated with ulcer disease and gastric cancer. The latter is one of the most prevalent malignancies and currently the fourth major cause of cancer-related deaths globally. The pathogen infects about 50% of the world population, and currently, no treatment ensures its total elimination. There has been an increase in our understanding of the pathophysiology and pathogenesis mechanisms of H. pylori over the years. H. pylori can induce several genetic alterations, express numerous virulence factors, and trigger diverse adaptive mechanisms during its adherence and colonization. For successful colonization and infection establishment, several effector proteins/toxins are released by the organism. Evidence is also available reporting spiral to coccoid transition as a unique tactic H. pylori uses to survive in the host’s gastrointestinal tract (GIT). Thus, the virulence and pathogenicity of H. pylori are under the control of complex interplay between the virulence factors, host, and environmental factors. Expounding the role of the various virulence factors in H. pylori pathogenesis and clinical outcomes is crucial for vaccine development and in providing and developing a more effective therapeutic intervention. Here we critically reflect on H. pylori infection and delineate what is currently known about the virulence and pathogenesis mechanisms of H. pylori .

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Heterogeneity of Helicobacter pylori Strains Isolated from Patients with Gastric Disorders in Guiyang, China

Cited by 11 publications

References 50 publications

Helicobacter pylori Virulence Factors and Clarithromycin Resistance-Associated Mutations in Mexican Patients

Helicobacter pylori Virulence Factors and Clarithromycin Resistance-Associated Mutations in Mexican Patients

Effective Eradication Regimen and Duration According to the Clarithromycin Susceptibility of Helicobacter pylori Determined Using Dual Priming Oligonucleotide-Based Multiplex Polymerase Chain Reaction

Helicobacter pylori: an up-to-date overview on the virulence and pathogenesis mechanisms

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