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Impact of Helicobacter pylori resistance to clarithromycin on the efficacy of the omeprazole–amoxicillin–clarithromycin therapy
Author(s) -
Tankovic J.,
Lamarque D.,
Lascols C.,
Soussy C. J.,
Delchier J. C.
Publication year - 2001
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.2001.00971.x
Subject(s) - clarithromycin , omeprazole , helicobacter pylori , proton pump inhibitor , amoxicillin , medicine , regimen , gastroenterology , drug resistance , antibiotics , microbiology and biotechnology , pharmacology , biology
Background: Helicobacter pylori resistance to clarithromycin is relatively frequent in France and is assumed to be the main cause of failure of the proton pump inhibitor–amoxicillin–clarithromycin (proton pump inhibitor–AC) therapy, which is the first‐line regimen in France. Aim: To determine the respective effects of clarithromycin primary and secondary resistances on efficacy of the proton pump inhibitor–AC regimen and to determine whether failures are associated with persistence of the same strain or with emergence of a new one. Methods: A total of 123 H. pylori ‐infected patients were treated for 7 days with omeprazole 20 mg b.d., amoxicillin 1 g b.d., and clarithromycin 500 mg b.d. Eradication was assessed by breath test in 102 patients. Minimal inhibitory concentrations of clarithromycin were determined by E ‐test. Strain genotyping was performed by random amplified polymorphic DNA. Results: The pre‐treatment and post‐treatment prevalences of clarithromycin resistance were 19% (23 out of 123) and 69% (nine out of 13), respectively. The rates of eradication were 68% (69 out of 102), 79% (67 out of 85), and 12% (two out of 17) for all, susceptible and resistant strains, respectively. The post‐treatment isolate was available for six patients with a susceptible pre‐treatment isolate and a persistent infection. Resistance emerged in two patients and was associated with persistence of the pre‐treatment strain in one and with selection of a new strain in the other. Conclusions: In our hospital, failures of the proton pump inhibitor–AC therapy are related to both clarithromycin primary and secondary resistances, but the emergence of secondary resistance does not explain all of the failures in the initial clarithromycin‐susceptible group. In that group a new strain can emerge after failure.