作者: M SUGIMOTO , T FURUTA , N SHIRAI , M IKUMA , A HISHIDA
DOI: 10.1016/J.CLPT.2006.03.007
关键词: Lansoprazole 、 CYP2C19 、 Biology 、 Gastritis 、 Helicobacter pylori 、 Clarithromycin 、 Omeprazole 、 Genotype 、 Proinflammatory cytokine 、 Immunology
摘要: Backgrounds and Aims Polymorphisms of proinflammatory cytokines, such as interleukin (IL) 1β tumor necrosis factor (TNF) α, are associated with individual differences in gastric mucosal inflammation acid inhibition response to Helicobacter pylori infection. We investigated whether inflammation-related cytokine polymorphisms would influence the eradication rates H by a triple-therapy regimen. Methods Three hundred sixty patients infected clarithromycin-sensitive strains were genotyped for IL1B −511, IL1RN, TNFA −857/−863/−1031, IL10 −1082/−819/−592, CYP2C19 underwent triple therapy 1 week proton pump inhibitor (20 mg omeprazole, 30 lansoprazole, or 10 rabeprazole) twice daily, 400 clarithromycin 750 amoxicillin (INN, amoxicilline) daily. The influences previously mentioned on analyzed. Results The intention-to-treat–based total rate was 83.6% (301/360). logistic regression analysis revealed that −511 independently rates, but other not these rates. C/C, C/T, T/T genotypes 72.2% (70/97), 87.7% (164/187), 88.2% (67/76), respectively (P = .0017). When stratified genotype status, genotype–dependent observed homozygous extensive metabolizers (EMs) heterozygous EMs poor CYP2C19. EM C/C quite low (51.1% [22/43]). Conclusions IL1B polymorphism, TNFA, is one determinants EMs. Clinical Pharmacology & Therapeutics (2006) 80, 41–50; doi:10.1016/j.clpt.2006.03.007