Commentaries

Helicobacter pylori resists arrest Testing for the presence of Helicobacter pylori and subsequent eradication of the infection is a key aspect in the management of dyspepsia, which is now the largest sin-gle area of cost for primary care in the United Kingdom.1 Since the bacterium was discovered in 1982 and its role in the aetiology of peptic ulcer disease became established, significant advances have been achieved in antimicrobial treatment with current regimens enabling successful eradi-cation in 85 to 90 % of patients.2 3 The reasons for treatment failure in the remaining small but significant group of infected individuals is often not clearly established but resistance to metronidazole and to clarithromycin are generally considered to be the primary factors. Both of these antibiotics are widely used in current regimens for eradicating H pylori although rates of resistance vary significantly from 10 to 50 % for metronidazole, and from 0 to 15 % for clarithromycin, depending on the population group surveyed.4 For instance, in a recent study of dyspep-tics attending an open access endoscopy clinic in mid-Essex, we found pretreatment rates of 6 % for clarithromycin and 37 % for metronidazole (L Teare, personal communication). The fact that resistance rates for clarithromycin may be gradually increasing is particularly worrying as it is a most useful antibiotic against H pylori because of its absorption and stability properties in the stomach. Consequently it is a key component in eradica-tion regimens, particularly those for first line treatment in areas of high prevalence of metronidazole resistance.3 The mode of action of clarithromycin after penetrating the cell wall is to bind to ribosomes and disrupt protein synthesis. Decrease in the binding of clarithromycin to the ribosome is linked to the development of resistance which in turn is attributed to various point mutations in the two 23S rRNA genes of H pylori. These mutations were first reported in US isolates in 1996 by Versalovic and colleagues5 and since then have been confirmed in clinical isolates from France,4 Sweden,6 Canada,7 and the Netherlands.8 The two most common mutations are those in which adenine residues are replaced by guanine at posi-

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