title: Low-dose intravenous pantoprazole for optimal inhibition of gastric acid in Korean patients.
abstract: OBJECTIVE
  Proton-pump inhibitor (PPI) therapy for bleeding ulcers is more efficacious in Asian patients than in non-Asian patients. The aim of this study was to evaluate the efficacy of various doses of pantoprazole on intragastric acidity in Korean patients.
  
  
  METHODS
  A prospective randomized study was conducted in 52 patients either with bleeding peptic ulcers after successful endotherapy or who received endoscopic mucosal resection for gastric neoplasms. Patients were randomized into two doses of intravenous pantoprazole: 40 mg q.d. and 40 mg b.i.d. We compared these results with our preliminary study utilizing high-dose pantoprazole (80 mg + 8 mg/h). The potential contribution of CYP2C19 genetic polymorphisms and the presence of Helicobacter pylori were also assessed.
  
  
  RESULTS
  Pantoprazole 40 mg b.i.d. and high-dose pantoprazole demonstrated better inhibition of intragastric acid than pantoprazole q.d. (P < 0.05). The pantoprazole 40 mg q.d. group exhibited significant variations in acid inhibition correlating with CYP2C19 genotype. Median 24 h pH values did not differ significantly between the pantoprazole b.i.d. and high-dose pantoprazole groups, regardless of H. pylori infection status. A median intragastric pH < 6.0 was observed in only three of 28 patients in the 40 mg b.i.d. group; these three patients were extensive metabolizers.
  
  
  CONCLUSIONS
  A 40 mg b.i.d. dose of pantoprazole is sufficient to maintain pH > 6.0 in Korean patients, except for patients with extensive metabolizing CYP2C19 genotypes.
authors.affiliation: Division of Gastroenterology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea.
authors.forename: Jung-Hwan
authors.initials: JH
authors.lastname: Oh
authors.forename: Myung-Gyu
authors.initials: MG
authors.lastname: Choi
authors.forename: Mi-Sook
authors.initials: MS
authors.lastname: Dong
authors.forename: Jae-Myung
authors.initials: JM
authors.lastname: Park
authors.forename: Chang-Nyol
authors.initials: CN
authors.lastname: Paik
authors.forename: Yu-Kyung
authors.initials: YK
authors.lastname: Cho
authors.forename: Jeong-Jo
authors.initials: JJ
authors.lastname: Jeong
authors.forename: In-Seok
authors.initials: IS
authors.lastname: Lee
authors.forename: Sang-Woo
authors.initials: SW
authors.lastname: Kim
authors.forename: Sok-Won
authors.initials: SW
authors.lastname: Han
authors.forename: Kyu-Yong
authors.initials: KY
authors.lastname: Choi
authors.forename: In-Sik
authors.initials: IS
authors.lastname: Chung
mesh_terms: D053799:2-Pyridinylmethylsulfinylbenzimidazoles / Q000008:administration & dosage / Q000627:therapeutic use*; D000328:Adult; D000368:Aged; D000897:Anti-Ulcer Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D001189:Aryl Hydrocarbon Hydroxylases / Q000235:genetics; D015992:Body Mass Index; D065731:Cytochrome P-450 CYP2C19; D004381:Duodenal Ulcer / Q000188:drug therapy / Q000235:genetics; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007275:Injections, Intravenous; D007723:Korea; D008297:Male; D008875:Middle Aged; D006899:Mixed Function Oxygenases / Q000235:genetics; D000077402:Pantoprazole; D011110:Polymorphism, Genetic; D011446:Prospective Studies; D013274:Stomach Neoplasms / Q000188:drug therapy / Q000235:genetics; D013276:Stomach Ulcer / Q000188:drug therapy / Q000235:genetics
chemical_list: D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000897:Anti-Ulcer Agents; D000077402:Pantoprazole; D006899:Mixed Function Oxygenases; D001189:Aryl Hydrocarbon Hydroxylases; C045793:CYP2C19 protein, human; D065731:Cytochrome P-450 CYP2C19