OBJECTIVES: To investigate the efficacies of two different triple-therapy regimens (standard versus low doses), and the influence of cytochrome P450 enzyme (CYP) genetic polymorphism on these efficacies, in Japanese patients undergoing Helicobacter pylori eradication treatment. METHODS: All patients received 1 week of triple therapy. Patients in group A (low-dose regimen) received omeprazole 40 mg/day + amoxicillin 1500 mg/day + clarithromycin 800 mg/day; patients in group B (standard-dose regimen) received omeprazole 40 mg/day + amoxicillin 2000 mg/day + clarithromycin 1000 mg/day. RESULTS: A total of 225 patients (113 in group A and 112 in group B) were randomised to one of the two triple-therapy regimens. The eradication rates were 78.8% (89/113 patients; 95% CI 70.1, 85.9) in group A and 83.0% (93/112 patients; 95% CI 74.8, 89.5) in group B. Genetic polymorphism of CYP2C19, a major metabolic enzyme of omeprazole, did not affect eradication rates, while susceptibility to clarithromycin greatly affected the success of eradication. The cumulative ulcer relapse rate at 24 weeks after endoscopically documented ulcer healing (30 weeks after completion of the drug regimen) was 8.3% for group A and 12.5% for group B (log rank test: p = 0.6248). However, comparison of the cumulative relapse rate of 6.7% in patients after successful H. pylori eradication with the relapse rate of 27.3% in those who failed H. pylori eradication revealed a significant difference in the remission-time curve (log rank test: p = 0.0047). This finding suggested the existence of a relationship between H. pylori eradication failure and ulcer relapse. Both drug regimens were well tolerated. Endoscopically proven reflux esophagitis developed in about 10% of patients after eradication, but was not clinically significant. CONCLUSIONS: One week of triple therapy with a low-dose regimen provides adequate H. pylori eradication in Japanese patients. CYP genetic polymorphism is of minimal clinical significance with both triple-therapy regimens.
RCT Entities:
OBJECTIVES: To investigate the efficacies of two different triple-therapy regimens (standard versus low doses), and the influence of cytochrome P450 enzyme (CYP) genetic polymorphism on these efficacies, in Japanese patients undergoing Helicobacter pylori eradication treatment. METHODS: All patients received 1 week of triple therapy. Patients in group A (low-dose regimen) received omeprazole 40 mg/day + amoxicillin 1500 mg/day + clarithromycin 800 mg/day; patients in group B (standard-dose regimen) received omeprazole 40 mg/day + amoxicillin 2000 mg/day + clarithromycin 1000 mg/day. RESULTS: A total of 225 patients (113 in group A and 112 in group B) were randomised to one of the two triple-therapy regimens. The eradication rates were 78.8% (89/113 patients; 95% CI 70.1, 85.9) in group A and 83.0% (93/112 patients; 95% CI 74.8, 89.5) in group B. Genetic polymorphism of CYP2C19, a major metabolic enzyme of omeprazole, did not affect eradication rates, while susceptibility to clarithromycin greatly affected the success of eradication. The cumulative ulcer relapse rate at 24 weeks after endoscopically documented ulcer healing (30 weeks after completion of the drug regimen) was 8.3% for group A and 12.5% for group B (log rank test: p = 0.6248). However, comparison of the cumulative relapse rate of 6.7% in patients after successful H. pylori eradication with the relapse rate of 27.3% in those who failed H. pylori eradication revealed a significant difference in the remission-time curve (log rank test: p = 0.0047). This finding suggested the existence of a relationship between H. pylori eradication failure and ulcer relapse. Both drug regimens were well tolerated. Endoscopically proven reflux esophagitis developed in about 10% of patients after eradication, but was not clinically significant. CONCLUSIONS: One week of triple therapy with a low-dose regimen provides adequate H. pylori eradication in Japanese patients. CYP genetic polymorphism is of minimal clinical significance with both triple-therapy regimens.
Authors: R W Van der Hulst; E A Rauws; B Köycü; J J Keller; M J Bruno; J G Tijssen; G N Tytgat Journal: Gastroenterology Date: 1997-10 Impact factor: 22.682
Authors: M Asaka; T Sugiyama; M Kato; K Satoh; H Kuwayama; Y Fukuda; T Fujioka; T Takemoto; K Kimura; T Shimoyama; K Shimizu; S Kobayashi Journal: Helicobacter Date: 2001-09 Impact factor: 5.753
Authors: S J Zanten; M Bradette; A Farley; D Leddin; T Lind; P Unge; E Bayerdörffer; R C Spiller; C O'Morain; P Sipponen; M Wrangstadh; L Zeijlon; P Sinclair Journal: Aliment Pharmacol Ther Date: 1999-03 Impact factor: 8.171
Authors: T Lind; S Veldhuyzen van Zanten; P Unge; R Spiller; E Bayerdörffer; C O'Morain; K D Bardhan; M Bradette; N Chiba; M Wrangstadh; C Cederberg; J P Idström Journal: Helicobacter Date: 1996-09 Impact factor: 5.753
Authors: P Unge; K Kimura; P Sipponen; P Ekström; K Satoh; M Hellblom; B Ohlin; A Stubberöd; K Kihira; T Yube; Y Yoshida Journal: Scand J Gastroenterol Date: 2003-05 Impact factor: 2.423
Authors: A Sapone; D Vaira; S Trespidi; F Perna; L Gatta; A Tampieri; C Ricci; G Cantelli-Forti; M Miglioli; G L Biagi; M Paolini Journal: Am J Gastroenterol Date: 2003-05 Impact factor: 10.864