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[Helicobacter pylori infection and antimicrobial agents resistance]

J-D de Korwin1

  • 1Service de médecine interne H, CHU de Nancy-hôpital central, 29, avenue de Lattre-de-Tassigny, 54035 Nancy, France. jd.dekorwin@chu-nancy.fr

La Revue De Medecine Interne
|January 23, 2004
PubMed
Abstract

Insights

Helicobacter pylori treatment failures are rising due to antimicrobial resistance. New DNA-based methods can detect resistance, guiding better treatment strategies for H. pylori infection.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Pharmacology

Background:

  • Standard seven-day triple therapies for Helicobacter pylori infection, using a proton pump inhibitor (PPI) and two antimicrobials (clarithromycin, amoxicillin, metronidazole), are increasingly failing.
  • Eradication failure rates, particularly in France, approach 30%, primarily driven by growing resistance to clarithromycin (macrolides) and metronidazole (nitro-imidazoles).
  • Primary clarithromycin resistance is around 10% globally (20% in France), significantly reducing eradication success. Secondary resistance contraindicates its use in second-line treatments. Amoxicillin and tetracycline resistance remain low (<2%). Metronidazole resistance is higher and impacts eradication rates, necessitating longer or alternative therapies.

Purpose of the Study:

  • To address the rising challenge of Helicobacter pylori treatment failures.
  • To highlight the impact of antimicrobial resistance on H. pylori eradication efficacy.
  • To explore advancements in detecting H. pylori resistance.

Main Methods:

  • Review of current knowledge on antimicrobial resistance patterns in H. pylori.
  • Analysis of factors contributing to eradication failures.
  • Discussion of emerging diagnostic methods for resistance detection.

Main Results:

  • Increasing primary and secondary resistance to key antibiotics like clarithromycin and metronidazole is a major cause of H. pylori treatment failure.
  • Resistance significantly reduces the effectiveness of standard triple therapies, necessitating modified or rescue regimens.
  • Novel diagnostic approaches based on bacterial DNA analysis are being developed.

Conclusions:

  • Understanding the genetic basis of H. pylori resistance is crucial for developing effective diagnostic tools.
  • DNA-based detection methods for clarithromycin resistance have been validated.
  • Future strategies will likely involve direct detection of resistance from gastric biopsies, improving personalized H. pylori treatment.

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