Cure of refractory duodenal ulcer and infection caused by Helicobacter pylori by high doses of omeprazole and amoxicillin in a homozygous CYP2C19 extensive metabolizer patient

Citation
T. Furuta et al., Cure of refractory duodenal ulcer and infection caused by Helicobacter pylori by high doses of omeprazole and amoxicillin in a homozygous CYP2C19 extensive metabolizer patient, CLIN PHARM, 67(6), 2000, pp. 684-689
Citations number
35
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Pharmacology,"Pharmacology & Toxicology
Journal title
CLINICAL PHARMACOLOGY & THERAPEUTICS
ISSN journal
0009-9236 → ACNP
Volume
67
Issue
6
Year of publication
2000
Pages
684 - 689
Database
ISI
SICI code
0009-9236(200006)67:6<684:CORDUA>2.0.ZU;2-W
Abstract
A 53-year old female patient with duodenal ulcer and Helicobacter pylori in fection was treated three times with a proton pump inhibitor-based triple t herapy, such as lansoprazole-clarithromycin-amoxicillin (INN, amoxicilline) and lansoprazole-minocycline-cefaclor: However, the H pylori infection was not cured. A culture test revealed that her infection was a clarithromycin -resistant but amoxicillin-sensitive strain of H pylori. Moreover, a polyme rase chain reaction-restriction fragment length polymorphism (PCR-RFLP) ana lysis revealed that she was a homozygous extensive metabolizer of cytochrom e P450 (CYP) 2C19 (wt/wt). The usual dose of the proton pump inhibitor was therefore assumed to be insufficient for her and then she was treated with a high dose of omeprazole (120 mg/day) and amoxicillin (2250 mg/day) for 2 weeks. The H pylori infection and the ulcer lesion were then cured. One of the factors associated with success or failure of cure of H pylori infectio n by the proton pump inhibitor-based triple therapy appeared to be CYP2C19 genotype status. Dual treatment with a sufficient dose of a proton pump inh ibitor plus amoxicillin could cure H pylori infection even after the failur e to cure H pylori infection by a usual proton pump inhibitor-based triple therapy in patients with the wt/wt homozygous extensive metabolizer genotyp e of CYP2C19.