Clarithromycin resistance and prevalence of Helicobacter pylori virulent genotypes in patients from Southern México with chronic gastritis

Alarcón‐Millán, Judit; Fernández‐Tilapa, Gloria; Cortés-Malagón, Enoc Mariano; Castañón-Sánchez, Carlos Alberto; Sampedro-Reyes, José De; Carmen, Iván Cruz-del; Betancourt-Linares, Reyes; Román-Román, Adolfo

doi:10.1016/j.meegid.2016.06.044

Cited by 37 publications

(24 citation statements)

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“…По последним данным, устойчивость H. pylori к кларитромицину увеличилась до 20-50% [11]. Большое количество работ объясняют устойчивость H. pylori к кларитромицину генотипом H. pylori [12]. Показано, что менее вирулентные CagA-негативные и VacA S2-содержащие штаммы связаны с первичной устойчивостью к кларитромицину [13].…”

Section: Discussionunclassified

Differentiated approach to eradication therapy in patients with chronic pancreatitis

Сарсенбаева

Домрачева

2020

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Purpose of the study. Compare the effectiveness of different eradication therapy regimens in patients with chronic pancreatitis with concomitant gastritis associated with various genetic variants of H. pylori.Materials and methods: 63 patients with chronic pancreatitis and concomitant Helicobacter pylori-associated gastritis were examined. The control group consisted of 45 patients with chronic gastritis. Diagnosis of chronic pancreatitis was based on anamnestic, clinical data, instrumental studies (MSCT). Diagnosis of H. pylori infection was carried out by the morphological method, 13C urease breath test, and immunoblotting. Statistical processing was carried out using application packages SPSS Statistic 17.0.Results. In patients with chronic pancreatitis, CagA-positive H. pylori strains were found 19.3% less often compared with the control group (p <0.05), VacA-positive—21.9% less often (p <0.05). In the study group, H. pylori genes encoding urease A production and genes encoding the synthesis of H. pylori outer membrane proteins (p33, p30, p29, p26, p19, p17) were significantly more frequently met. In the group of patients with chronic pancreatitis, the standard triple therapy of the 1st line with the inclusion of bismuth tripotassium dicitrate was 86.8% more effective (p <0.01) compared to the standard triple therapy of the 1st line, and the maximum increase in efficiency was observed among owners of H. pylori strains, expressing urease A and with the representation on the outer membrane of the proteins p30, p33, p26, p19, p17 (p <0.01).Conclusion. Eradication therapy in patients with chronic pancreatitis in the presence of pathogenicity complex p30, p33, urease A, p26, p19, p17 in H. pylori according to the standard line triple therapy protocol with the inclusion of bismuth tripotassium dicitrate has advantages compared to the standard triple therapy protocol 1 line (p <0.001).

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Section: Discussionunclassified

Differentiated approach to eradication therapy in patients with chronic pancreatitis

Сарсенбаева

Домрачева

2020

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“…A significant and welcome increase was noted over the last year in the number of studies addressing the important topic of antimicrobial resistance in H. pylori infection. These are summarized in Table . A key message emerging is the relentless rise in antibiotic resistance, especially to clarithromycin and levofloxacin.…”

Section: Antimicrobial Resistancementioning

confidence: 99%

Treatment of Helicobacter pylori infection 2017

et al. 2017

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Over the last decade, it has been widely reported that the success of Helicobacter pylori eradication treatment is falling. A steady decline was observed in the number of patients achieving eradication with standard first-line triple therapy of two antibiotics and a proton pump inhibitor [1][2][3]. It now appears that the first-line eradication therapies most commonly used in everyday clinical practice fall considerably short of the 80% intention-to-treat (ITT) eradication rates that are considered the minimal acceptable levels as recommended in the Maastricht guidelines [4]. Interestingly, two studies emerged from Asian centers in the last 12 months, which show that, in this part of the world at least, eradication levels using standard therapies remain close to 80%. A Malaysian study showed a standard 1-week pantoprazole, amoxycillin, and clarithromycin regimen to be well tolerated and highly efficacious with a per-protocol eradication rate of 84% [5]. A Japanese study showed remarkably consistent per-protocol eradication rates from 2001 to 2009 fluctuating between 75 and 78% for standard 7-day triple-therapy regimens [6]. A limit of many studies especially those including clarithromycin or levofloxacin is that H. pylori susceptibility to the drugs, which is the main prediction of failure, was not tested. LevofloxacinThe use of levofloxacin as a first-line therapy has been examined in great depth in the last year. Levofloxacin may be used as a substitute for clarithromycin in either a standard triple or sequential regimen. A large study comparing the antibiotics in either regimen shows a clear advantage to levofloxacin in both combinations. Per-protocol cure rates for triple therapy were 66% for omeprazole-clarithromycin-amoxycillin compared with 83% for omeprazole-levofloxacin-amoxycillin and 81% for omeprazole-amoxycillin-clarithromycin-metronidazole vs 85% for omeprazole-amoxycillin-levofloxacinmetronidazole, with no difference in compliance rates or adverse events [7]. It has been proposed that sequential levofloxacin-based regimens are of most benefit in areas where clarithromycin resistance is in excess of 15%, and another study in such an area showed eradication rates of 81% with clarithromycin sequential therapy compared with 96% with levofloxacin sequential therapy. A third arm in this study looked at the dose of levofloxacin required and illustrated no benefit in increasing the dose from 250 to 500 mg [8]. Indeed, another study went so far as to suggest that once-daily dosing of a levofloxacin-based triple regimen may be as efficacious as twice daily [9]. The literature from Asia also seems to support levofloxacin as a good alternative first-line therapy. A study on a triple regimen showed per-protocol eradication rates of 78% for standard clarithromycin-containing therapies compared with 83% for a levofloxacin-based regimen [10]. Another study from the Middle East looked at whether combining clarithromycin and levofloxacin in the same regimen could be Keywords Peptic ulcer disease, resistance, compli...

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“…The rising rate of CLA resistance, particularly in H pylori , is mostly due to drug target site alterations ( via base substitutions), 20,21 drug efflux enhancement, 22 and biofilm formation 23,24 . Base substitutions mostly occur in domain V of 23S rRNA, predominantly A2142G and A2143G 25,26 of H pylori , equivalent to A2058G and A2059G in E coli 27 …”

Section: Introductionmentioning

confidence: 99%

The outward shift of clarithromycin binding to the ribosome in mutantHelicobacter pyloristrains

et al. 2020

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Objectives Disruption of protein synthesis, by drug‐mediated restriction of the ribosomal nascent peptide exit tunnel (NPET), may inhibit bacterial growth. Here, we have studied the secondary and tertiary structures of domain V of the 23S rRNA in the wild‐type and mutant (resistant) H. pylori strains and their mechanisms of interaction with clarithromycin (CLA). Methods H pylori strains, isolated from cultured gastric biopsies, underwent CLA susceptibility testing by E test, followed by PCR amplification and sequencing of domain V of 23S rRNA. The homology model of this domain in H pylori, in complex with L4 and L22 accessory proteins, was determined based on the E. coli ribosome 3D structure. The interactions between CLA and 23S rRNA complex were determined by molecular docking studies. Results Of the 70 H pylori strains, isolated from 200 dyspeptic patients, 11 (16%) were CLA‐resistant. DNA sequencing identified categories with no (A), A2142G (B), and A2143G (C) mutations. Docking studies of our homology model of 23S rRNA complex with CLA showed deviated positions for categories B and C, in reference to category A, with 12.19 Å and 7.92 Å RMSD values, respectively. In both mutant categories, CLA lost its interactions at positions 2142 and 2587 and gained two new bonds with the L4 accessory protein. Conclusion Our data suggest that, in mutant H pylori strains, once the nucleotides at positions 2142 and 2587 are detached from the drug, CLA interacts with and is peeled back by the L4 accessory protein, removing the drug‐imposed spatial restriction of the NPET.

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Clarithromycin resistance and prevalence of Helicobacter pylori virulent genotypes in patients from Southern México with chronic gastritis

Cited by 37 publications

References 63 publications

Differentiated approach to eradication therapy in patients with chronic pancreatitis

Differentiated approach to eradication therapy in patients with chronic pancreatitis

Treatment of Helicobacter pylori infection 2017

The outward shift of clarithromycin binding to the ribosome in mutantHelicobacter pyloristrains

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