Abstract

Discovered in the last decade, Heliobacter pylori is now known to play a role in the onset of chronic gastritis and peptic ulcer and also to be strongly associated with gastric cancer and MucosaAssociated Lymphoid Tissue (MALT) lymphoma [1,2]. These findings have revolutionized the therapeutical approach to gastric pathology. Moreover, the wide spread of dyspeptic symptoms has contributed to the development of a variety of noninvasive diagnostic assays, such as the urea breath test, serologic and whole blood tests, most of which are available to the primary care physicians for the rapid diagnosis of H. pylori infection. As a consequence, antibiotic eradication therapy has been widely applied, often without endoscopic examination which is essential for the identification of the cause of the gastric pathophysiological disturbances. At present, the most commonly used treatment is the triple therapy: a proton pump inhibitor and two antibiotics (metronidazole plus clarithromycin, or amoxycillin plus clarithromycin, or metronidazole plus amoxycillin) [3]. Because of the abuse of this therapeutic scheme, a consistent increase in metronidazole and clarithromycin resistance among H. pylori strains has been monitored [4,5]. Recently the first case of an amoxycillin-resistant H. pylori strain has also been reported [6]. The appearance of resistant strains is one of the major causes of treatment failure [7]. Thus, monitoring the prevalence of resistant strains and establishing the local susceptibility level to the commonly used drugs is at least as important as the development of new antimicrobial agents. For this reason and because of the high incidence of gastric cancer in our region [8,9] (the southern part of Switzerland together with the northern part of Italy) we collected 142 H. pylori strains from different patients living in the Cantone Ticino (southern part of Switzerland) in 1996 and 1997. These strains were tested for susceptibility to metronidazole, clarithromycin and amoxycillin. Minimum inhibitory concentrations (MICs) of 142 H. pylori strains were determined using the E-test method (AB Biodisk, Solna, Sweden) according to the manufacturer’s instructions. The MIC breakpoint values for H. pylori resistance were chosen according to the available data published in the literature: 8 mg/L for both metronidazole and clarithromycin, and 2 mg/L

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