N Vakil1, B Hahn, D McSorley. 1. University of Wisconsin Medical School, Milwaukee 53233, USA.
Abstract
BACKGROUND: Clarithromycin is a key component of several antimicrobial treatment regimens for Helicobacter pylori. Cure rates with clarithromycin-containing regimens are significantly decreased when resistance is present. Resistance develops by a point mutation in the ribosomal RNA of some organisms exposed to clarithromycin. We studied the prevalence of clarithromycin-resistant organisms in patients with duodenal ulcer in the United States from 1993-96. METHODS: Patients with endoscopic evidence of a duodenal ulcer were studied. Gastric biopsies were cultured for H. pylori and antimicrobial sensitivity was determined by the E-test (epsilometer agar diffusion gradient). RESULTS: In 1993-94, three of 78 patients (4%) had clarithromycin-resistant strains of H. pylori. In 1995-96, 44 of 348 patients (12.6%; p = 0.025) had resistant strains of H. pylori. Patients who had previously failed antimicrobial treatment for H. pylori accounted for much of the increase in resistant strains (25%). CONCLUSIONS: Failed therapy with clarithromycin-based regimens is a growing cause of antimicrobial resistance in H. pylori in the United States. Whereas the overall rates of primary resistance are low, the increase in secondary resistance over a short period of time is worrisome. New treatments that prevent the emergence of resistance may be important in the future.
BACKGROUND:Clarithromycin is a key component of several antimicrobial treatment regimens for Helicobacter pylori. Cure rates with clarithromycin-containing regimens are significantly decreased when resistance is present. Resistance develops by a point mutation in the ribosomal RNA of some organisms exposed to clarithromycin. We studied the prevalence of clarithromycin-resistant organisms in patients with duodenal ulcer in the United States from 1993-96. METHODS:Patients with endoscopic evidence of a duodenal ulcer were studied. Gastric biopsies were cultured for H. pylori and antimicrobial sensitivity was determined by the E-test (epsilometer agar diffusion gradient). RESULTS: In 1993-94, three of 78 patients (4%) had clarithromycin-resistant strains of H. pylori. In 1995-96, 44 of 348 patients (12.6%; p = 0.025) had resistant strains of H. pylori. Patients who had previously failed antimicrobial treatment for H. pylori accounted for much of the increase in resistant strains (25%). CONCLUSIONS: Failed therapy with clarithromycin-based regimens is a growing cause of antimicrobial resistance in H. pylori in the United States. Whereas the overall rates of primary resistance are low, the increase in secondary resistance over a short period of time is worrisome. New treatments that prevent the emergence of resistance may be important in the future.
Authors: M Matsumura; Y Hikiba; K Ogura; G Togo; I Tsukuda; K Ushikawa; Y Shiratori; M Omata Journal: J Clin Microbiol Date: 2001-02 Impact factor: 5.948
Authors: M Kato; Y Yamaoka; J J Kim; R Reddy; M Asaka; K Kashima; M S Osato; F A El-Zaatari; D Y Graham; D H Kwon Journal: Antimicrob Agents Chemother Date: 2000-08 Impact factor: 5.191