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  5. CYP2C19 genotypes in the pharmacokinetics/pharmacodynamics of proton pump inhibitor-based therapy of Helicobacter pylori infection
 
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CYP2C19 genotypes in the pharmacokinetics/pharmacodynamics of proton pump inhibitor-based therapy of Helicobacter pylori infection

Journal
Expert Opinion on Drug Metabolism and Toxicology
Journal Volume
6
Journal Issue
1
Pages
29-41
Date Issued
2010
Author(s)
JYH-CHIN YANG  
CHUN-JUNG LIN  
DOI
10.1517/17425250903386251
URI
https://www.scopus.com/inward/record.uri?eid=2-s2.0-72949117415&doi=10.1517%2f17425250903386251&partnerID=40&md5=cdf1359dab28cfb801b61114c59cf569
https://scholars.lib.ntu.edu.tw/handle/123456789/565074
Abstract
Importance of the field: Proton pump inhibitors (PPIs) are potent gastric acid inhibitors. Therapies with a PPI and antibiotics are used to cure Helicobacter pylori (H. pylori) infection, which is closely related to many gastrointestinal diseases. Most PPIs are mainly metabolized by cytochrome 2C19 (CYP2C19). The genetic polymorphisms of CYP2C19 may lead to the differences in pharmacokinetics (PK), pharmacodynamics (PD) and clinical efficacy of PPIs. Areas covered in this review: The roles of PPIs on the eradication of H. pylori are summarized. The impact f CYP2C19 polymorphism on the PK and PD of PPIs is addressed and related to the present status of therapy for H. pylori infection. The opinions on the strategy of PPIs-based therapies of H. pylori infection are provided. What the reader will gain: Update the factors that may influence the PPIs-based therapies of H. pylori infection. Take home message: The eradication rates of H. pylori infection are significantly different between patients who are CYP2C19 extensive metabolizers and poor metabolizers, partly because of the differences in the PK and PD of PPIs. Nonetheless, the differences can be improved by adjusting the regimens of PPIs and using antibiotics that have less H. pylori-resistance. ? 2010 Informa UK Ltd.
SDGs

[SDGs]SDG3

Other Subjects
amoxicillin; bismuth; clarithromycin; cytochrome P450 2C19; dexlansoprazole; diazepam; esomeprazole; furazolidone; lansoprazole; levofloxacin; metronidazole; omeprazole; pantoprazole; phenytoin; proton pump inhibitor; rabeprazole; rifabutin; tetracycline; timoprazole; tinidazole; unclassified drug; antibiotic resistance; antibiotic therapy; area under the curve; clinical trial; Clostridium difficile infection; constipation; diarrhea; DNA polymorphism; dosage schedule comparison; drug bioavailability; drug blood level; drug dose comparison; drug dose increase; drug dose sequence; drug efficacy; drug eruption; drug half life; drug induced headache; drug megadose; drug metabolism; drug potency; drug structure; genetic variability; genotype; Helicobacter infection; Helicobacter pylori; human; maximum plasma concentration; nausea; pharmacogenetics; review; single drug dose; stomach pH; sustained drug release; time to maximum plasma concentration; Aryl Hydrocarbon Hydroxylases; Genotype; Helicobacter Infections; Helicobacter pylori; Humans; Proton Pump Inhibitors; Helicobacter pylori
Type
review

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