Proton pump inhibitor- and clarithromycin-based triple therapies for Helicobacter pylori eradication

Vieira, Régis Rodrigues; Fontes, Luis Eduardo Santos; Pacheco, Rafael Leite; Fernandes, Marcos Ap; Malta, Paloma P; Riera, Rachel

doi:10.1002/14651858.cd013734

Cited by 4 publications

(4 citation statements)

References 22 publications

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“…If not treated adequately, a gastric ulcer may lead to serious complications, such as perforation and bleeding, or may progress toward gastric cancer with substantial morbidity and mortality rates (Thrift et al 2023). Inhibition of acid secretion using proton pump inhibitors and eradication of H. pylori by treatment with clarithromycin, tinidazole, and lansoprazole (or omeprazole), are currently the most widely used therapeutic regimens for gastric ulcer (Vieira et al 2020). However, with the side effects of these therapeutic agents, the emerging resistance of H. pylori to antibiotics (Boyanova et al 2023), and the high recurrence rate of gastric ulcers, efforts are being directed toward the identi cation of new therapeutic modalities.…”

Section: Introductionmentioning

confidence: 99%

Effects of some anti-ulcer and anti-inflammatory natural products on cyclooxygenase and lipoxygenase enzymes: insights from in silico analysis

Metuge,

Betow,

Bekono

et al. 2024

Preprint

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Gastric and duodenal ulcers are increasingly becoming global health burdens. The side effects of conventional treatments such as non-steroid anti-inflammatory drugs (NSAIDs), proton pump inhibitors (PPIs), antibiotics, histamine H2 receptor antagonists (H2RAs), and cytoprotective agents have necessitated the search for new medications. Plants are a rich source of active metabolites and herbal medicines have been used in the treatment of ulcers and cancers. In this study, we used in silico methods to evaluate the effects of some anti-ulcer and anti-inflammatory phytochemicals on some key enzymes, cyclooxygenase (COX), and lipoxygenase (LOX) which are implicated in the protection and destruction of the gastric mucosa. Five compounds, rhamnetin, kaempferol, rutin, rosmarinic acid, and chlorogenic acid were identified to putatively bind to cyclooxygenase 2 (COX-2) and 5-lipoxygenase (5-LOX) but not to cyclooxygenase 1 (COX-1). The interaction mechanisms between these phytochemicals and the target proteins are discussed. The drug metabolism, pharmacokinetics, and toxicity of the compounds have been evaluated to assess their suitability as potential next-generation anti-ulcer and anti-inflammatory drugs.

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Section: Introductionmentioning

confidence: 99%

Effects of some anti-ulcer and anti-inflammatory natural products on cyclooxygenase and lipoxygenase enzymes: insights from in silico analysis

Metuge,

Betow,

Bekono

et al. 2024

Preprint

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“…Clarithromycin, a macrolide antibiotic, is still an effective antibiotic used in many H . pylori treatment regimens [ 24 ]. Clarithromycin interacts with 50S ribosomal subunit of H .…”

Section: Introductionmentioning

confidence: 99%

“…Clarithromycin-based triple treatment remains the therapy of choice for treating H. pylori infection [23]. Clarithromycin, a macrolide antibiotic, is still an effective antibiotic used in many H. pylori treatment regimens [24]. Clarithromycin interacts with 50S ribosomal subunit of H. pylori, leading to the suppressing of protein synthesis and resulting in a bacteriostatic effect [25].…”

Section: Introductionmentioning

confidence: 99%

Exposure of Helicobacter pylori to clarithromycin in vitro resulting in the development of resistance and triggers metabolic reprogramming associated with virulence and pathogenicity

Rosli,

Al-Maleki,

Loke

et al. 2024

PLoS ONE

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In H. pylori infection, antibiotic-resistance is one of the most common causes of treatment failure. Bacterial metabolic activities, such as energy production, bacterial growth, cell wall construction, and cell-cell communication, all play important roles in antimicrobial resistance mechanisms. Identification of microbial metabolites may result in the discovery of novel antimicrobial therapeutic targets and treatments. The purpose of this work is to assess H. pylori metabolomic reprogramming in order to reveal the underlying mechanisms associated with the development of clarithromycin resistance. Previously, four H. pylori isolates were induced to become resistant to clarithromycin in vitro by incrementally increasing the concentrations of clarithromycin. Bacterial metabolites were extracted using the Bligh and Dyer technique and analyzed using metabolomic fingerprinting based on Liquid Chromatography Quadrupole Time-of-Flight Mass Spectrometry (LC-Q-ToF-MS). The data was processed and analyzed using the MassHunter Qualitative Analysis and Mass Profiler Professional software. In parental sensitivity (S), breakpoint isolates (B), and induced resistance isolates (R) H. pylori isolates, 982 metabolites were found. Furthermore, based on accurate mass, isotope ratios, abundances, and spacing, 292 metabolites matched the metabolites in the Agilent METLIN precise Mass-Personal Metabolite Database and Library (AM-PCDL). Several metabolites associated with bacterial virulence, pathogenicity, survival, and proliferation (L-leucine, Pyridoxone [Vitamine B6], D-Mannitol, Sphingolipids, Indoleacrylic acid, Dulcitol, and D-Proline) were found to be elevated in generated resistant H. pylori isolates when compared to parental sensitive isolates. The elevated metabolites could be part of antibiotics resistance mechanisms. Understanding the fundamental metabolome changes in the course of progressing from clarithromycin-sensitive to breakpoint to resistant in H. pylori clinical isolates may be a promising strategy for discovering novel alternatives therapeutic targets.

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“…It causes a variety of gastrointestinal disorders, such as gastritis, gastric ulcer, and duodenal ulcer, and is also associated with gastric cancer [ 2 ]. The standard triple therapy for H. pylori infection includes a proton pump inhibitor (PPI) and two antibiotics (amoxicillin with clarithromycin, or metronidazole) [ 3 ]. However, misuse and overuse of antimicrobials is causing the steady growth in antibiotic resistance and is severely hindering the eradication of H. pylori .…”

Section: Introductionmentioning

confidence: 99%

Polymorphism of virulence genes and biofilm associated with in vitro induced resistance to clarithromycin in Helicobacter pylori

Rosli,

Al-Maleki,

Loke

et al. 2023

Gut Pathog

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Background Clarithromycin-containing triple therapy is commonly used to treat Helicobacter pylori infections. Clarithromycin resistance is the leading cause of H. pylori treatment failure. Understanding the specific mutations that occur in H. pylori strains that have evolved antibiotic resistance can help create a more effective and individualised antibiotic treatment plan. However, little is understood about the genetic reprogramming linked to clarithromycin exposure and the emergence of antibiotic resistance in H. pylori. Therefore, this study aims to identify compensatory mutations and biofilm formation associated with the development of clarithromycin resistance in H. pylori. Clarithromycin-sensitive H. pylori clinical isolates were induced to develop clarithromycin resistance through in vitro exposure to incrementally increasing concentration of the antibiotic. The genomes of the origin sensitive isolates (S), isogenic breakpoint (B), and resistant isolates (R) were sequenced. Single nucleotide variations (SNVs), and insertions or deletions (InDels) associated with the development of clarithromycin resistance were identified. Growth and biofilm production were also assessed. 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.

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Proton pump inhibitor- and clarithromycin-based triple therapies for Helicobacter pylori eradication

Abstract: To assess the e ectiveness and safety of proton pump inhibitor-and clarithromycin-based triple therapies for Helicobacter pylori (H. pylori) eradication. Proton pump inhibitor-and clarithromycin-based triple therapies for Helicobacter pylori eradication (Protocol)

Cited by 4 publications

References 22 publications

Effects of some anti-ulcer and anti-inflammatory natural products on cyclooxygenase and lipoxygenase enzymes: insights from in silico analysis

Effects of some anti-ulcer and anti-inflammatory natural products on cyclooxygenase and lipoxygenase enzymes: insights from in silico analysis

Exposure of Helicobacter pylori to clarithromycin in vitro resulting in the development of resistance and triggers metabolic reprogramming associated with virulence and pathogenicity

Polymorphism of virulence genes and biofilm associated with in vitro induced resistance to clarithromycin in Helicobacter pylori

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