[Influence of CYP2C19 polymorphism and Helicobacter pylori status on the antisecretory effect of omeprazole in gastroesophageal reflux disease].

BACKGROUND/AIMS The acid suppressive effect of omeprazole (OMP) is influenced by the metabolic capacity of gastric acid suppression, which is dependent on CYP2C19 polymorphism. The aim of this study was to determine the influence of CYP2C19 polymorphism and Helicobacter pylori (H. pylori) infection on the intragastric acid suppression of OMP. METHODS Thirty one patients with gastroesophageal reflux disease were treated with a daily oral dose of 20 mg OMP for 28 days. Patients were genotyped for CYP2C19 polymorphism by polymerase chain reaction-restriction fragment length polymorphism and classified into three groups: homogenous extensive metabolizers (Ho-EMs), heterogenous extensive metabolizers (Ht-EMs) and poor metabolizer (PMs). H. pylori infection status were assessed before OMP treatment. Intragastric pH was monitored over twenty four-hours before (day 0) and after (day 29) the treatment with OMP. RESULTS Twenty four-hour intragastric mean pH in the PMs group was significantly higher than those in Ho-EMs and Ht-EMs (5.3+/-1.3 vs. 2.8+/-0.6, 3.6+/-1.4) (p<0.005). Twenty four-hour intragastric mean pH after the administration of OMP in the H. pylori positive group was significantly higher than the H. pylori negative group (4.7+/-1.4 vs. 3.2+/-1.4) (p<0.001). There was no significant difference in acid suppressive activity of OMP between H. pylori positive and negative group according to CYP2C19 polymorphism. CONCLUSIONS The acid suppressive effect of OMP on intragastric pH is dependent on CYP2C19 polymorphism and the H. pylori-infected status in patients with gastroesophageal reflux disease. H. pylori infection may play a role in enhancing the acid suppressive potential of OMP.