Clarithromycin-Resistant Genotypes and Eradication of <i>Helicobacter pylori</i>

Francesco, Vincenzo De; Margiotta, M.; Zullo, Angelo; Hassan, Cesare; Troiani, Laura; Burattini, Osvaldo; Stella, Francesca; Leo, Alfredo Di; Russo, Francesco; Marangi, Stefania; Monno, Rosa; Stoppino, V.; Morini, Sergio; Panella, C.; Ierardi, Enzo

doi:10.7326/0003-4819-144-2-200601170-00006

Cited by 197 publications

(170 citation statements)

References 35 publications

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“…Previous studies have suggested that the presence of the A2143G mutation confers a significantly decreased H. pylori eradication potential when using clarithromycin-containing regimens, more so than the presence of the A2142C or A2142G mutations. 24 At this time, the clinical manifestations and current therapies for each are identical and there is no utility for differentiation between the strains in the clinical laboratory setting. However, differentiation of mutations may have importance in future epidemiological studies or as recommendations for antimicrobial therapies change.…”

Section: Discussionmentioning

confidence: 99%

PCR detection of clarithromycin-susceptible and -resistant Helicobacter pylori from formalin-fixed, paraffin-embedded gastric biopsies

et al. 2013

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Antimicrobial resistance to clarithromycin is a growing concern in the treatment of Helicobacter pylori and is associated with three major point mutations of the 23S rRNA, A2142C, A2142G, and A2143G. The use of traditional culture-based methods for determination of clarithromycin resistance in H. pylori are time consuming and lack sensitivity. We implemented a real-time PCR with melt curve analysis to detect and characterize H. pylori in formalin-fixed, paraffin-embedded gastric biopsy specimens to assess the frequency of clarithromycin resistance mutations in our study population. One hundred and fifty-three formalin-fixed, paraffin-embedded gastric biopsies were chosen on the basis of positive immunohistochemical staining for H. pylori and an accompanying histopathological diagnosis of Helicobacter-associated gastritis. New adjacent sections were taken for immunohistochemical staining and DNA extraction with subsequent testing by PCR assay and melt curve analysis using a primer and probe combination first described by Oleastro et al. 12 One hundred and forty-six samples demonstrated adequate amplification of a human DNA control target. Of these, there were 122 H. pylori immunohistochemistry-positive samples. In all, 103 out of 122 (84%) immunohistochemistry-positive samples demonstrated amplifiable H. pylori 23S rRNA gene target and 19 (16%) demonstrated no amplification of H. pylori. Twenty-two samples were negative for H. pylori by immunohistochemistry and PCR. Two were negative for H. pylori by immunohistochemistry, but were positive for H. pylori by PCR. In all, 52 out of 105 (50%) PCR-positive samples demonstrated resistance mutations, and it was determined that a heterogeneous population of mutated and unmutated organisms was present in 11 out of 52 samples. The use of PCR assays allows for a timely assessment of clarithromycin resistance status without the disadvantages of culture-based methods, and may lead to a decrease in treatment failure rates.

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Section: Discussionmentioning

confidence: 99%

PCR detection of clarithromycin-susceptible and -resistant Helicobacter pylori from formalin-fixed, paraffin-embedded gastric biopsies

et al. 2013

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“…The T2183C and A2223G mutations have been frequently found to be the cause of observed CAM resistance, while the A2143G mutation, which has a much stronger impact than the A2142G and A2142C [18]. mutations responsible for 90% of primary CAM-resistant H. pylori cases isolated in Western countries [19], accounted only for 23% of resistant strains in Asia [19].…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori antibiotic susceptibility patterns in Bangladesh: Emerging levofloxacin resistance

Aftab

Miftahussurur

Subsomwong

et al. 2016

J Infect Dev Ctries

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Introduction: The most recent study to report Helicobacter pylori antibiotic resistance rates in Bangladesh was published 15 years ago and did not include levofloxacin. We therefore aimed to determine the current antibiotic susceptibility of H. pylori to amoxicillin, clarithromycin, metronidazole, tetracycline and levofloxacin in Bangladesh. Methodology: This study included 133 consecutive patients who underwent endoscopy examination at Dhaka Medical College in November 2014. The serial two-fold agar dilution method was used to determine the minimum inhibitory concentrations of the five antibiotics. Results: Among 56 cultured strains, H. pylori showed high rates of resistance to clarithromycin and metronidazole (39.3% and 94.6%, respectively). Moreover, levofloxacin showed an emerging antimicrobial resistance pattern (66.1%), which was higher in patients with gastritis than that in those with peptic ulcers (p = 0.02). The resistance rate of levofloxacin was significantly higher in patients living in Dhaka city compared to those living in the village (p = 0.049). However, amoxicillin and tetracycline resistance rates were very low. Resistance to both metronidazole and levofloxacin was most commonly observed. Conclusions: The rates of resistance to clarithromycin, metronidazole, and levofloxacin were high in Bangladesh, which suggests that triple therapy based on these drugs may not be useful as first-line therapies in Bangladesh. Alternative strategies such as furazolidone-based triple therapy, bismuth-based quadruple therapies, or sequential therapy may be more effective for patients in in Bangladesh.

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“…This regimen includes a PPI and amoxicillin for 5 d, followed by a PPI, clarithromycin, and tinidazole triple therapy for another 5 d. Several studies have indicated that the eradication rate of sequential therapy was significantly higher than that of STT [85][86][87] . The reason that sequential therapy has a higher eradication rate than STT is that amoxicillin and PPI administered during the first 5 d decreases H. pylori density in the stomach, which increases clarithromycin and metronidazole efficacy [32,[88][89][90] . In addition, amoxicillin damages the bacterial cell wall and limits production of an efflux channel underlying drug resistance.…”

Section: Are There Suitable Sequential and Concomitant Therapy Alternmentioning

confidence: 99%

“…Clarithromycin resistance is due to three point mutations at A2142C, A2142G, and A2143G in the 23s rRNA gene [31] . In particular, the A2143G mutation has been related to a very low eradication rate [32] . In contrast, the A2143G mutation occurs in only 23% of resistant strains in Eastern countries [31] .…”

Section: Current Antibiotic Resistance In Worldwidementioning

confidence: 99%

Antibiotic treatment forHelicobacter pylori: Is the end coming?

Kim

Choi

Chung

2015

WJGPT

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Infection with the Gram-negative pathogen Helicobacter pylori (H. pylori ) has been associated with gastroduodenal disease and the importance of H. pylori eradication is underscored by its designation as a group I carcinogen. The standard triple therapy consists of a proton pump inhibitor, amoxicillin and clarithromycin, although many other regimens are used, including quadruple, sequential and concomitant therapy regimens supplemented with metronidazole, clarithromycin and levofloxacin. Despite these efforts, current therapeutic regimens lack efficacy in eradication due to antibiotic resistance, drug compliance and antibiotic degradation by the acidic stomach environment. Core tip: This article reviews the recent literature describing antibiotic resistance and trends in Helicobacter pylori (H. pylori ) treatment. As there is no effective conventional therapy, new treatments are being developed and bismuth quadruple, sequential, concomitant therapies are recommended as a first-line regimen in regions with high levels of clarithromycin resistance. Quinolones have also been used for H. pylori treatment, although the cure rate has gradually reduced with this approach. New therapeutic directions include probiotic supplementation, tailored therapy, novel agents, and nanotechnology.

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Clarithromycin-Resistant Genotypes and Eradication of Helicobacter pylori

Abstract: The A2143G mutation seemed to be associated with a very low eradication rate. The sequential regimen achieved a higher cure rate than standard therapy even in patients with these strains.

Cited by 197 publications

References 35 publications

PCR detection of clarithromycin-susceptible and -resistant Helicobacter pylori from formalin-fixed, paraffin-embedded gastric biopsies

PCR detection of clarithromycin-susceptible and -resistant Helicobacter pylori from formalin-fixed, paraffin-embedded gastric biopsies

Helicobacter pylori antibiotic susceptibility patterns in Bangladesh: Emerging levofloxacin resistance

Antibiotic treatment forHelicobacter pylori: Is the end coming?

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