Abstract
BackgroundCurrent available treatments for Helicobacter pylori eradication are chosen according to local clarithromycin and metronidazole resistance prevalence. The aim of this study was to estimate, by means of molecular methods, both clarithromycin and metronidazole resistance in gastric mucosa from patients infected with H.pylori.MethodsA total of 191 DNA samples were analyzed. DNA was purified from gastric mucosa obtained from patients who underwent an upper gastrointestinal endoscopy at an university hospital from Santiago, Chile, between 2011 and 2014. H.pylori was detected by real-time PCR. A 5’exonuclease assay was developed to detect A2142G and A2143G mutations among H.pylori-positive samples. rdxA gene was sequenced in samples harboring A2142G and A2143G mutations in order to detect mutations that potentially confer dual clarithromycin and metronidazole resistance.ResultsNinety-three (93) out of 191 DNA samples obtained from gastric mucosa were H.pylori-positive (48.7%). Clarithromycin-resistance was detected in 29 samples (31.2% [95%CI 22.0–41.6%]). The sequencing of rdxA gene revealed that two samples harbored truncating mutations in rdxA, one sample had an in-frame deletion, and 11 had amino acid changes that likely cause metronidazole resistance.ConclusionsWe estimated a prevalence of clarithomycin-resistance of 31.8% in Santiago, Chile. Three of them harbor inactivating mutations in rdxA and 11 had missense mutations likely conferring metronidazole resistance. Our results require further confirmation. Nevertheless, they are significant as an initial approximation in re-evaluating the guidelines for H.pylori eradication currently used in Chile.
Highlights
Current available treatments for Helicobacter pylori eradication are chosen according to local clarithromycin and metronidazole resistance prevalence
Mutations in the peptidyltransferase region encoded in domain V of 23S rRNA are responsible for macrolide resistance [3]
Epidemiological studies evaluating regional clarithromycin resistance have been conducted based on detection of A2142G and A2143G in DNA isolated from gastric biopsies [4, 5]
Summary
Current available treatments for Helicobacter pylori eradication are chosen according to local clarithromycin and metronidazole resistance prevalence. The aim of this study was to estimate, by means of molecular methods, both clarithromycin and metronidazole resistance in gastric mucosa from patients infected with H.pylori. Epidemiological studies evaluating regional clarithromycin resistance have been conducted based on detection of A2142G and A2143G in DNA isolated from gastric biopsies [4, 5]. Commercial tests detecting both mutations are available [3], performing at a sensitivity rate of > 94% and a specificity rate of > 98.5% compared to the culture susceptibility test. Only Garrido and Toledo [7] have evaluated primary resistance of H.pylori to clarithromycin in clinical isolates from Santiago, Chile.
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