title: CYP2C19 genotype-related efficacy of omeprazole for the treatment of infection caused by Helicobacter pylori.
abstract: OBJECTIVE
  Omeprazole is used for the treatment of infection caused by Helicobacter pylori, and it is metabolized by the polymorphic cytochrome P4502C19 (CYP2C19). We have found that the anti-H pylori efficacy by the combination of omeprazole and antibiotics is related to the CYP2C19 genotype.
  
  
  METHODS
  One hundred eight patients with cultured H pylori-positive gastritis or peptic ulcer were treated with three regimens: quadruple treatment without proton pump inhibitors (n = 25), dual treatment with omeprazole and amoxicillin (INN, amoxicilline) (n = 26), and triple treatment with omeprazole, amoxicillin, and clarithromycin (n = 57). The CYP2C19 genotype was determined by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method and the assessment of the eradication of H pylori was based on all negative examinations, including culture, histology, and 13C-urea breath test.
  
  
  RESULTS
  The eradication rates for the extensive metabolizers were 50% and 86% for the dual and triple treatments, respectively. In contrast, all of the poor metabolizers treated with omeprazole and antibiotics (n = 15) showed an eradication of H pylori.
  
  
  CONCLUSIONS
  The anti-H pylori effect of dual treatment is highly efficient for CYP2C19 poor metabolizers, which suggests that clarithromycin is not necessary as a first line of therapy for this type of patients. Genotyping can provide a choice for the optimal regimen based on individual CYP2C19 genotype.
authors.affiliation: Department of Hospital Pharmacy, School of Medicine, Kobe University, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Tanigawara
authors.forename: N
authors.initials: N
authors.lastname: Aoyama
authors.forename: T
authors.initials: T
authors.lastname: Kita
authors.forename: K
authors.initials: K
authors.lastname: Shirakawa
authors.forename: F
authors.initials: F
authors.lastname: Komada
authors.forename: M
authors.initials: M
authors.lastname: Kasuga
authors.forename: K
authors.initials: K
authors.lastname: Okumura
mesh_terms: D000658:Amoxicillin / Q000627:therapeutic use; D000863:Antacids / Q000627:therapeutic use; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D000897:Anti-Ulcer Agents / Q000494:pharmacology*; D001189:Aryl Hydrocarbon Hydroxylases; D001729:Bismuth / Q000627:therapeutic use; D017291:Clarithromycin / Q000627:therapeutic use; D065731:Cytochrome P-450 CYP2C19; D065607:Cytochrome P-450 Enzyme Inhibitors; D003577:Cytochrome P-450 Enzyme System / Q000235:genetics*; D004359:Drug Therapy, Combination; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D005756:Gastritis / Q000188:drug therapy* / Q000382:microbiology; D005838:Genotype; D016481:Helicobacter Infections / Q000188:drug therapy* / Q000382:microbiology; D016480:Helicobacter pylori / Q000187:drug effects*; D006635:Histamine H2 Antagonists / Q000627:therapeutic use; D006801:Humans; D008795:Metronidazole / Q000627:therapeutic use; D006899:Mixed Function Oxygenases / Q000037:antagonists & inhibitors* / Q000235:genetics*; D009853:Omeprazole / Q000494:pharmacology*; D010406:Penicillins / Q000627:therapeutic use; D010437:Peptic Ulcer / Q000188:drug therapy* / Q000382:microbiology; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D011500:Protein Synthesis Inhibitors / Q000627:therapeutic use; D016896:Treatment Outcome
chemical_list: D000863:Antacids; D000900:Anti-Bacterial Agents; D000897:Anti-Ulcer Agents; D065607:Cytochrome P-450 Enzyme Inhibitors; D004791:Enzyme Inhibitors; D006635:Histamine H2 Antagonists; D010406:Penicillins; D011500:Protein Synthesis Inhibitors; D008795:Metronidazole; D000658:Amoxicillin; D003577:Cytochrome P-450 Enzyme System; D006899:Mixed Function Oxygenases; D001189:Aryl Hydrocarbon Hydroxylases; C045793:CYP2C19 protein, human; D065731:Cytochrome P-450 CYP2C19; D017291:Clarithromycin; C010804:bismuth subnitrate; D009853:Omeprazole; D001729:Bismuth