{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,4]],"date-time":"2026-06-04T09:12:54Z","timestamp":1780564374328,"version":"3.54.1"},"reference-count":37,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2016,11,2]],"date-time":"2016-11-02T00:00:00Z","timestamp":1478044800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Hacettepe University Scientific Research Center","award":["013 D10 101 001"],"award-info":[{"award-number":["013 D10 101 001"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Basic Clin Pharma Tox"],"published-print":{"date-parts":[[2017,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Pantoprazole is a proton pump inhibitor that is commonly used in the treatment of peptic ulcer disease (<jats:styled-content style=\"fixed-case\">PUD<\/jats:styled-content>) and metabolized by cytochrome P450 (<jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>) enzymes<jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>2C19 and<jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>3A4. Pantoprazole is a substrate for multi\u2010drug resistance protein 1 (<jats:styled-content style=\"fixed-case\">MDR<\/jats:styled-content>1). Single nucleotide polymorphisms (<jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content>s) in<jats:italic><jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>2C19<\/jats:italic>,<jats:italic><jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>3A4<\/jats:italic>and<jats:italic><jats:styled-content style=\"fixed-case\">MDR<\/jats:styled-content>1<\/jats:italic>affect enzyme activity or gene expression of proteins and may alter plasma pantoprazole concentrations and treatment success in<jats:styled-content style=\"fixed-case\">PUD<\/jats:styled-content>. In this study, we aimed to investigate the association between genetic polymorphisms in<jats:italic><jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>2C19<\/jats:italic>,<jats:italic><jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>3A4<\/jats:italic>and<jats:italic><jats:styled-content style=\"fixed-case\">MDR<\/jats:styled-content>1<\/jats:italic>and pharmacokinetics of pantoprazole and therapeutic outcome in patients with either<jats:italic>Helicobacter pylori<\/jats:italic>\u2010associated [H.P.(+)]\u2010<jats:styled-content style=\"fixed-case\">PUD<\/jats:styled-content>or [H.P.(+)]\u2010gastritis. The plasma pantoprazole concentrations were determined by using an<jats:styled-content style=\"fixed-case\">HPLC<\/jats:styled-content>method at the third hour after a 40\u2010mg tablet of pantoprazole administration in 194 newly diagnosed patients with either [H.P.(+)]\u2010<jats:styled-content style=\"fixed-case\">PUD<\/jats:styled-content>or [H.P.(+)]\u2010gastritis. Genotyping was performed by using<jats:styled-content style=\"fixed-case\">PCR<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">RFLP<\/jats:styled-content>and<jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content>sequencing. Among patients appearing for follow\u2010up examination (n = 105), the eradication rate for<jats:italic>H. pylori<\/jats:italic>was 82.8% (n = 87). The median pantoprazole plasma concentrations in poor metabolizers (<jats:styled-content style=\"fixed-case\">PM<\/jats:styled-content>), rapid metabolizers (<jats:styled-content style=\"fixed-case\">RM<\/jats:styled-content>) and ultrarapid metabolizers (<jats:styled-content style=\"fixed-case\">URM<\/jats:styled-content>) were 2.07, 1.69 and 1.28 \u03bcg\/ml, respectively (<jats:italic>p<\/jats:italic>= 0.04).<jats:italic><jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>3A4*1G<\/jats:italic>and<jats:italic>*22<\/jats:italic>polymorphisms did not affect plasma pantoprazole concentrations and<jats:italic>H. pylori<\/jats:italic>eradication rate. The<jats:styled-content style=\"fixed-case\">MDR<\/jats:styled-content>1 genetic polymorphisms did not affect plasma pantoprazole concentrations.<jats:italic><jats:styled-content style=\"fixed-case\">MDR<\/jats:styled-content>1 3435<jats:styled-content style=\"fixed-case\">CC<\/jats:styled-content>\u20102677<jats:styled-content style=\"fixed-case\">GG<\/jats:styled-content>\u20101236<jats:styled-content style=\"fixed-case\">CC<\/jats:styled-content><\/jats:italic>haplotype carriers had lower<jats:italic>H. pylori<\/jats:italic>eradication rate (60%) than the remaining subjects (84.9%) while the difference was not statistically significant (<jats:italic>p<\/jats:italic>= 0.07). In conclusion, while<jats:italic><jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>2C19<\/jats:italic>genetic polymorphisms significantly affected plasma pantoprazole concentrations, polymorphisms of<jats:italic><jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>2C19<\/jats:italic>,<jats:italic><jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>3A4<\/jats:italic>and<jats:italic><jats:styled-content style=\"fixed-case\">MDR<\/jats:styled-content>1<\/jats:italic>did not affect<jats:italic>H. pylori<\/jats:italic>eradication rates.<\/jats:p>","DOI":"10.1111\/bcpt.12667","type":"journal-article","created":{"date-parts":[[2016,9,9]],"date-time":"2016-09-09T19:47:03Z","timestamp":1473450423000},"page":"199-206","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Effects of Genetic Polymorphisms of Cytochrome P450 Enzymes and<scp>MDR<\/scp>1 Transporter on Pantoprazole 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