Molecular Assessment of Resistance to Clarithromycin in <i>Helicobacter pylori</i> Strains Isolated from Patients with Dyspepsia by Fluorescent In Situ Hybridization in the Center of Iran

Vazirzadeh, Jina; Falahi, Jamal; Moghim, Sharareh; Narimani, Tahmineh; Rafiei, Rahmatollah; Karbasizade, Vajihe

doi:10.1155/2020/2304173

Cited by 19 publications

(16 citation statements)

References 29 publications

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“…3 The most frequent and well-studied molecular pathway for clarithromycin resistance is due to A2142G and A2143G point mutations in domain V of the 23S rRNA gene. 4 Other mutations like A2142C, G1939A, A2115G, G2141A, A2144G, A2144T, C2147G, T2182C, G2224A, and T2215C vary geographically and found to mediate resistance phenotype. 1,3,5 This study on the characterization of 23S rRNA gene mutations in clinical isolates of H. pylori in Pakistan found three new features of domain V. First, a new MboII RFLP pattern was found.…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Characterization of Domain V Mutations in Clinical Isolates of Helicobacter pylori in Pakistan and Their Effect on Clarithromycin MIC

Anis¹,

Niaz²

2021

IDR

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Purpose: Clarithromycin is commonly prescribed for H. pylori infection. Domain V mutations are responsible for clarithromycin resistance. This study was aimed to characterize the clarithromycin resistance and its associated mutations in clinical isolates of H. pylori in Pakistan. Materials and Methods: Infection was diagnosed in 93 patients' biopsies using culture, rapid urease test, 16S rRNA, and vacA gene multiplex PCR. Clarithromycin resistance was assessed by the agar dilution method. Mutations were detected by PCR-RFLP using 46 (1.4 kb) domain V fragments. Sequencing was executed for 13 domain V fragments, of which 12 showed unusual amplicon size (1.2 kb) and 01 had a new MboII RFLP pattern. Results: A total of 48 (83%) strains were obtained from 58 (62.3%) PCR H. pylori-positive samples. Resistance (MIC ≥ 0.001 mg/mL) and intermediate resistance phenotype (MIC = 0.0005 mg/mL) was observed in 22 (46%), and 10 (21%) isolates, respectively. The primary resistance was found in 23 (39.6%) samples. PCR-RFLP detected A2142G, A2143G, and double mutations in 19, 04, and 01 resistant strain, respectively. Sequencing of 10 amplicons obtained from intermediated resistant strains and 03 amplicons from resistant strains showed 138 new mutations. Among them, T2182C was also seen in 04 intermediated resistant isolates, whereas A2142G, A2143G, and A2143C were observed in resistant isolates. The new MboII RFLP pattern in an intermediated resistant strains was due to A1761G mutation. Conclusion: H. pylori domain V mutations showed extensive diversity. Multiple mutations in domain V may give endurance to H. pylori against clarithromycin. Further investigations on the molecular mechanism of antibiotic resistance in H. pylori seem crucial at this stage.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Characterization of Domain V Mutations in Clinical Isolates of Helicobacter pylori in Pakistan and Their Effect on Clarithromycin MIC

Anis¹,

Niaz²

2021

IDR

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“…This has a blocking effect on the link between the antibiotic and the ribosome, and consequently, protein synthesis is not inhibited by the drug. Furthermore, mutations have also been found in A2143G, A2144G, A2143C, and T2182C, which cause resistance to clarithromycin in H. pylori strains [130,131].…”

Section: The Diagnosis Over Timementioning

confidence: 99%

“…The first study in 1990 confirmed that the cure for duodenal ulcer will be healing from the H. pylori infection, and in 1992, trials for proposed vaccines started. In 1994, the first trials with PPI triple therapies for ulcer treatment began; in 1996, the Maastricht I Consensus Report (and later, the other report), screen-and-treat strategy was proposed over time, and in 2010, the bismuth quadruple therapies were revisited [23,24,130]. All patients with gastric or duodenal ulcers who are positive for H. pylori should receive primary treatment for the eradication of the bacterium, which is based on a proton pump inhibitor and is given in combination with two antibiotics for 7 days.…”

Section: New Therapeutic Issuesmentioning

confidence: 99%

40 Years of Helicobacter pylori: A Revolution in Biomedical Thought

Charitos

D’Agostino

Topi

et al. 2021

Gastroenterology Insights

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Background: Various microorganisms such as bacteria, virus, and fungi can infect humans and cause not just a simple infection but septic conditions, organ dysfunction, and precancerous conditions or cancer involving various organ systems. After the discovery of the microscope, it was easier to discover and study such microorganisms, as in the case of Helicobacter pylori, a pathogen that was seen in the distant era of the nineteenth century but without being recognized as such. It took 100 years to later discover the pathogenesis and the cancer that this bacterium can cause. Since it was discovered, until today, there has been a continuous search for the understanding of its pathogenetic mechanisms, and the therapeutic approach is continuously updated. Methods: We investigated how diagnosis and therapy were dealt with in the past and how researchers sought to understand, exactly, the pathogenetic biomolecular mechanisms of H. pylori, from the genesis of the infection to the current knowledge, with an analysis of carcinogenic mechanisms in the stomach. We have examined the scientific evolution of the knowledge of the disease over these 40 years in the gastroenterological and pharmacological fields. This was possible through a search in the databases of Medline, the WHO website, the Centers for Disease Control and Prevention (CDC) website, PubMed, and Web of Science to analyze the earlier and the latest data regarding H. pylori. Results: With the scientific discoveries over time, thanks to an increasing number of progressions in scientific research in the analysis of the gastric mucosa, the role of Helicobacter pylori in peptic ulcer, carcinogenesis, and in some forms of gastric lymphoma was revealed. Furthermore, over the years, the biomolecular mechanism involvement in some diseases has also been noted (such as cardiovascular ones), which could affect patients positive for H. pylori. Conclusions: Thanks to scientific and technological advances, the role of the bacterium H. pylori in carcinogenesis has been discovered and demonstrated, and new prospective research is currently attempting to investigate the role of other factors in the stomach and other organs. Cancer from H. pylori infection had a high incidence rate compared to various types of cancer, but in recent years, it is improving thanks to the techniques developed in the detection of the bacterium and the evolution of therapies. Thus, although it has become an increasingly treatable disease, there is still continuous ongoing research in the field of treatment for resistance and pharma compliance. Furthermore, in this field, probiotic therapy is considered a valid adjuvant.

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“…A culture-based method is difficult as H pylori is a fastidious organism capable of growing only under a narrow set of conditions. Resistance to clarithromycin of H pylori was associated with point mutations of the V domain of the 23S rRNA gene in the 50S subunit that decreases the affinity of drug binding to the ribosome, 22 and PCR-RFLP method has been developed to detect these point mutations. PCR-RFLP method has expressed a reliable assay allowing cost-effective and rapid detection of clarithromycin-resistant strains.…”

Section: Number Of Patients Percentmentioning

confidence: 99%

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

2021

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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 clarithromycinresistant 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.How to cite this article: Nyi KN, Soe AM, Htut ZM. Molecular detection of genotypic clarithromycin-resistant strains and its effect on the eradication rate of concomitant therapy in

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Molecular Assessment of Resistance to Clarithromycin in Helicobacter pylori Strains Isolated from Patients with Dyspepsia by Fluorescent In Situ Hybridization in the Center of Iran

Cited by 19 publications

References 29 publications

Characterization of Domain V Mutations in Clinical Isolates of Helicobacter pylori in Pakistan and Their Effect on Clarithromycin MIC

Characterization of Domain V Mutations in Clinical Isolates of Helicobacter pylori in Pakistan and Their Effect on Clarithromycin MIC

40 Years of Helicobacter pylori: A Revolution in Biomedical Thought

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

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