Aims: PPI are metabolised by the polymorphic CYP2C19. H.pylori eradication results according to different PPIs and dosages are inconsistent. Data from asian studies suggested that poor metabolisers of PPIs do better, data in caucasians are scarce. Objective/Methods: Meta-analysis of available literature data. Results: By mid of 2003, 12 studies met the inclusion criteria and reported differences in eradication outcome between wt/wt (wildtype, extensive metabolisers) vs. combined wt/mt and mt/mt (mutant, deficient metabolisers) alleles. Significant (p=0.0012) heterogeneity could be observed and was resolved (p=0.23) by excluding 4 rabeprazole studies. 8 studies were based on racemic omeprazole or lansoprazole (see figure displayed). No bias was noted (Funnel diagrams). 1) All studies: DerSimonian-Laird pooled risk difference=0.1361, approximate 95%CI=0.0666 to 0.2055, p=0.0001 2) Omeprazole/ Lansoprazole studies (figure): DerSimonian-Laird pooled risk difference=0.1828, approximate 95%CI=0.1176 to 0.2480, p<0.0001 This absolute risk difference between wildtype and CYP2C19 mutant patients of around 20% translates into a low NNT of 6. Conclusions: Genotypic differences in CYP2C19 status affect H. pylori eradication rates in Caucasian patients as well as Asian patients if racemic omeprazole or lansoprazole is used (as both are mainly metabolised by CYP2C19). Testing for CYP2C19 genotypes appears to be clinically relevant–independently from antibiotic resistance–as about 20% lower eradication rates must be expected in wildtype patients, who represent two-third of Caucasian populations.
Key words
CYP2C19 - Eradikation - Helicobacter pylori - Metaanalyse - Metabolisierung - Protonenpumpenhemmer
