Infection à Helicobacter pylori : bonnes pratiques

Mégraud, Françis

doi:10.1016/j.lpm.2010.04.004

Cited by 12 publications

(2 citation statements)

References 18 publications

(17 reference statements)

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“…It is widely accepted that Helicobacter pylori , a Gram negative microaerophylic bacterium, is involved in several clinical digestive tract conditions such as chronic gastritis, peptic and duodenal ulcers, gastric cancer and lymphoproliferative disorders [ 1 ]. Treatment of H. pylori infection results in ulcer healing and in a reduction of the risk of gastric cancer and lymphoma [ 2 , 3 ].…”

Section: Introductionmentioning

confidence: 99%

Low Helicobacter pylori primary resistance to clarithromycin in gastric biopsy specimens from dyspeptic patients of a city in the interior of São Paulo, Brazil

Suzuki

Lopes

et al. 2013

BMC Gastroenterol

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BackgroundClarithromycin, amoxicillin, and a pump proton inhibitor are the most common drugs recommended as first-line triple therapy for H.pylori treatment, which results in eradication rates close to 80%, varying regionally, principally due to emergency cases and increases of clarithromycin resistant strains. Nucleotide substitutions at the H. pylori domain V of the 23S rRNA fraction are involved in the macrolide resistance and the A2142G and A2143G mutations are predominant in clinical isolates worldwide including in Brazil. As H. pylori culture is fastidious, we investigated the primary occurrence of H. pylori A2142G and A2143G rDNA 23S mutations using a molecular approach directly on gastric biopsies of dyspeptic patients consecutively attended at Hospital das Clinicas of Marilia, São Paulo, Brazil.MethodsBiopsy specimens obtained from 1137 dyspeptic patients, were subjected to histopathology and H. pylori diagnosis by histology and PCR. PCR/RFLP assay was used to detect A2142G and A2143G point mutations at domain V of the H. pylori 23S rDNA associated with clarithromycin resistance. Through the developed assay, a 768 bp PCR amplicon corresponding to1728 to 2495 bp of the 23S H. pylori rDNA is restricted with MboII for A2142G mutation detection and with BsaI for A2143G mutation detection. Occurrence of 23S rDNA A2142G results in two DNA fragments (418 and 350 bp) and of 23S rDNA A2143G results in three DNA fragments (108, 310 and 350pb), due to a conserved BsaI restriction site.ResultsThe PCR method used to diagnose H. pylori presented sensitivity, specificity and accuracy of 77,6%, 79,3% and 78,6%, respectively, compared to histology, the gold standard method for H. pylori diagnosis used in our routine. Prevalence of H.pylori with clarithromycin resistant genotypes was 2,46%, with predominance of A2143G 23S rDNA point mutation.ConclusionsThe PCR/RFLP assay was a rapid and accurate H.pylori diagnostic and clarithromycin resistance determination method useful for routine practice. As prevalence of primary resistance of H.pylori to clarithromycin due to A2142G and A2143G mutations remains low in Marilia, the standard clarithromycin containing triple therapy is still valid.

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Section: Introductionmentioning

confidence: 99%

Low Helicobacter pylori primary resistance to clarithromycin in gastric biopsy specimens from dyspeptic patients of a city in the interior of São Paulo, Brazil

Suzuki

Lopes

et al. 2013

BMC Gastroenterol

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“…It is widely accepted that Helicobacter pylori , a Gram negative microaerophilic bacterium, is associated with several digestive tract diseases such as chronic gastritis, peptic and duodenal ulcers, gastric cancer and lymphoproliferative disorders [1]. There is no standardized treatment regimen for H.pylori infection [2] and once the bacterium is detected in altered gastric mucosa, the indicated treatment consists of a triple antibiotic regimen including metronidazole, clarithromycin, amoxicillin, tinidazole, tetracycline and fluoroquinolones associated with a proton pump inhibitor such as omeprazole, lansoprazole or pantoprazole [3-5], according to antibiotic prescription policies for local medical care.…”

Section: Introductionmentioning

confidence: 99%

Absence of Helicobacter pylori high tetracycline resistant 16S rDNA AGA926-928TTC genotype in gastric biopsy specimens from dyspeptic patients of a city in the interior of São Paulo, Brazil

2012

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BackgroundTreatment effectiveness of Helicobacter pylori varies regionally and is decreasing worldwide, principally as a result of antibiotic resistant bacterium. Tetracycline is generally included in second line H. pylori eradication regimens. In Brazil, a high level of tetracycline resistance (TetR) is mainly associated with AGA926-928TTC 16 S rDNA nucleotide substitutions. As H. pylori culture is fastidious, we investigated the primary occurrence of H. pylori 16 S rDNA high level TetR genotype using a molecular approach directly on gastric biopsies of dyspeptic patients attending consecutively at Hospital das Clinicas of Marilia, São Paulo, Brazil.MethodsGastric biopsy specimens of 68 peptic ulcer disease (PUD) and 327 chronic gastritis (CG) patients with a positive histological diagnosis of H. pylori were investigated for TetR 16 S rDNA genotype through a molecular assay based on amplification of a 16 S rDNA 545 bp fragment by polymerase chain reaction and HinfI restriction fragment length polymorphism (PCR/RFLP). Through this assay, AGA926-928TTC 16 S rDNA TetR genotype resulted in a three DNA fragment restriction pattern (281, 227 and 37 bp) and its absence originated two DNA fragments (264 and 281 bp) due to a 16 S rDNA conserved Hinf I restriction site.ResultsThe 545 bp 16 S rDNA PCR fragment was amplified from 90% of gastric biopsies from histological H. pylori positive patients. HinfI RFLP revealed absence of the AGA926–928TTC H. pylori genotype and PCR products of two patients showed absence of the conserved 16 S rDNA HinfI restriction site. BLASTN sequence analysis of four amplicons (two conserved and two with an unpredicted HinfI restriction pattern) revealed a 99% homology to H. pylori 16 S rDNA from African, North and South American bacterial isolates. A nucleotide substitution abolished the conserved HinfI restriction site in the two PCR fragments with unpredicted HinfI RFLP, resulting in an EcoRI restriction site.ConclusionsH. pylori AGA926-928TTC 16 S rDNA gene substitutions were not found in our population. More research is required to investigate if H. pylori TetR has a different genetic background in our region and if the nucleotide substitutions of the uncultured H. pylori 16 S rRNA partial sequences have biological significance.

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Quand rechercher Helicobacter pylori et comment l’éradiquer: techniques de recherche, traitements, vérification de l’éradication

Delchier

2011

Acta Endosc

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Infection à Helicobacter pylori : bonnes pratiques

Cited by 12 publications

References 18 publications

Low Helicobacter pylori primary resistance to clarithromycin in gastric biopsy specimens from dyspeptic patients of a city in the interior of São Paulo, Brazil

Low Helicobacter pylori primary resistance to clarithromycin in gastric biopsy specimens from dyspeptic patients of a city in the interior of São Paulo, Brazil

Absence of Helicobacter pylori high tetracycline resistant 16S rDNA AGA926-928TTC genotype in gastric biopsy specimens from dyspeptic patients of a city in the interior of São Paulo, Brazil

Quand rechercher Helicobacter pylori et comment l’éradiquer: techniques de recherche, traitements, vérification de l’éradication

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