Abstract

BackgroundResistance of Helicobacter pylori to clarithromycin has been associated with A2142G and A2143G point mutations in the 23S rRNA gene. Thus, the purpose of the present study was to determine the prevalence of each mutation in 52 clarithromycin-resistant H. pylori strains and to characterize the influence each type of mutation on the MIC.MethodsThe MIC for clarithromycin was determined by the agar dilution method, and the point mutations of H. pylori were detected by PCR followed by restriction fragment length polymorphism.ResultsClarithromycin MICs ranged from 2 to >256 microgram ml-1 among the 52 strains included in this study. Both the A2142G and the A2143G mutations were present in 94.2% of clarithromycin-resistant H. pylori strains examined. A relationship was observed between the presence of the A2142G mutation and the highest MIC values (p = 0.01).ConclusionIn an H. pylori-infected population, the A2142G mutation may incur to a greater probability of treatment failure if clarithromycin is used.

Highlights

  • Resistance of Helicobacter pylori to clarithromycin has been associated with A2142G and A2143G point mutations in the 23S rRNA gene

  • Detection of mutation associated with clarithromycin resistance The point mutations of H. pylori were detected by PCR followed by restriction fragment length polymorphism (RFLP)

  • Part of the 23S rRNA gene was amplified with primers 18 (5'AGTCGGGACCTAAGGCGAG-3') and 21 (5'-TTCCCGCTTAGATGCTTTCAG-3'), and the amplicon of approximately 1.4 Kb was digested with MboII (New England Biolabs, Beverly, MA, USA) or BsaI (New England Biolabs) to detect the A2142G and the A2143G mutations, respectively [8]

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Summary

Introduction

Resistance of Helicobacter pylori to clarithromycin has been associated with A2142G and A2143G point mutations in the 23S rRNA gene. The purpose of the present study was to determine the prevalence of each mutation in 52 clarithromycin-resistant H. pylori strains and to characterize the influence each type of mutation on the MIC. The bacteria can be eradicated in up to 90% of patients, side effects, poor compliance and resistance to the antibiotics used are common causes of treatment failure [3,4]. The mechanism of resistance to clarithromycin in H. pylori seems to be due to a decrease in binding of macrolides to the ribosome, associated with point mutations within the peptidyltransferaseencoding region of 23S rRNA gene [7,8]. The purpose of the present (page number not for citation purposes)

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