ANTIMICROBIAL RESISTANCE IN HELICOBACTER-PYLORI - A GLOBAL OVERVIEW

Helicobacter pylori resistance to antimicrobial agents is of particula r concern because it is a major determinant in the failure of eradicat ion regimens. Antimicrobial drug resistance has been reported to occur for nitroimidazoles, macrolides, fluoroquinolones, rifampin and tetra cyclines. Resistance to nitroimidazoles is the most common, in the ran ge of 30-40% on the average in Europe while the overall prevalence rat e of resistance to macrolides is lower, probably ranging between 2-10% in most countries. Development of secondary (acquired) resistance to nitroimidazoles and to the macrolides usually occurs as a rule (> 70-1 00%) in case of failed eradication therapy. Data available from severa l centres seems however to indicate that a significant shift towards i ncreasing resistance to metronidazole and to the macrolides might have possibly occurred in many countries over the last years. Resistances to both metronidazole and to clarithromycin are the most significant o nes because they influence the success of the treatments although this seems to be less marked and more dependent on the treatment regimens considered in the case of metronidazole resistance than in the setting of clarithromycin resistance. These differences may in part relate to methodological variations and to the inherent difficulties in assessi ng the susceptibility of H. pylori to metronidazole. It is possible th at different resistance cut-off might also have to be considered for m etronidazole depending on the treatment regimens administered. The mec hanisms of resistance have been well defined for the macrolides and ar e beginning to be unraveled for the nitroimidazoles. In all cases, res istance of H. pylori to antimicrobial agent seems to be due to the dev elopment of single mutational events in chromosomal genes rather than to the acquisition of exogeneous resistance genes. Owing to the restri cted ability of microbiology laboratories with expertise in H. pylori culture and the lack of standardised methodology for susceptibility te sting, H. pylori culture is not often performed routinely. It should h owever be considered after documented treatment failure or fn patients from a geographic area or of an ethnic origin with higher likelihood of antimicrobial drug resistance. Likewise it is deemed very important to institute national and regional surveillance programs to follow th e evolution of H. pylori resistance and to better adapt treatment regi mens to changes in resistance patterns.