Abstract
Proton pump inhibitors (PPI) are widely used for the treatment of gastroesophageal reflux disease (GERD), and in combination with antibiotics for the treatment of Helicobacter pylori infection. PPI are mainly metabolized by the polymorphic cytochromes P450 2C19 and 3A4. Genetic polymorphisms of these genes with resulting different enzyme activities may have an impact on the clinical efficacy of PPI-based therapies. There is increasing evidence that in Asian patient populations the efficacy of PPI-based eradication therapies is influenced by the patients CYP2C19 metabolizer status. Also two European studies report on CYP2C19-dependent eradication rates of H. pylori. In slow metabolizers, the AUC of oral PPI are higher in comparison to extensive metabolizers resulting in a stronger suppression of intragastric acid secretion. Recent studies suggest that the healing rate of erosive GERD is also influenced by the CYP2C19 metabolizer status. This review focuses on the relationship between CYP2C19 polymorphisms and clinical outcome after PPI based therapies in H. pylori eradication and GERD.
Keywords: Cytochrome P450, proton pump inhibitor, Helicobacter pylori, gastroesophageal reflux disease