genotype–related efficacy of omeprazole for the treatment of infection caused by

Tanigawara, Yusuke; Aoyama, Nobuo; Kita, Tomoko; Shirakawa, Kiyoshi; Komada, Fusao; Kasuga, Masato; Okumura, Katsuhiko

doi:10.1016/s0009-9236(99)70017-2

Cited by 172 publications

(123 citation statements)

References 24 publications

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“…A series of clinical studies on the CYP2C19 genotype and the pharmacokinetics and pharmacodynamics of three proton pump inhibitors (PPIs), omeprazole, lansoprazole and rabeprazole, were conducted to establish the individualized pharmacotherapy based on the CYP2C19 genotyping. [1][2][3][4][5] The subjects were classified into homo extensive metabolizers, hetero extensive metabolizers and poor metabolizers according to the CYP2C19 genotype diagnosed. The findings were summarized as follows: 1) plasma concentrations of omeprazole and lansoprazole after single oral administration were defined by the CYP2C19 genotype, whereas rabeprazole was not, 2) the CYP2C19 genotype-dependency of lansoprazole was weaker than omeprazole, and 3) hetero extensive metabolizers could be included with homo extensive metabolizers to be extensive metabolizers.…”

mentioning

confidence: 99%

Different Contribution of CYP2C19 in the in Vitro Metabolism of Three Proton Pump Inhibitors.

Kita

Sakaeda

Baba

et al. 2003

Biological & Pharmaceutical Bulletin

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Inter-individual variation in the pharmacokinetics and thereby pharmacodynamics of many therapeutic agents are possibly caused by genetic polymorphisms of drug metabolizing enzymes including cytochrome P450 2C9 (CYP2C9), CYP2C19 and CYP2D6. A series of clinical studies on the CYP2C19 genotype and the pharmacokinetics and pharmacodynamics of three proton pump inhibitors (PPIs), omeprazole, lansoprazole and rabeprazole, were conducted to establish the individualized pharmacotherapy based on the CYP2C19 genotyping. [1][2][3][4][5] The subjects were classified into homo extensive metabolizers, hetero extensive metabolizers and poor metabolizers according to the CYP2C19 genotype diagnosed. The findings were summarized as follows: 1) plasma concentrations of omeprazole and lansoprazole after single oral administration were defined by the CYP2C19 genotype, whereas rabeprazole was not, 2) the CYP2C19 genotype-dependency of lansoprazole was weaker than omeprazole, and 3) hetero extensive metabolizers could be included with homo extensive metabolizers to be extensive metabolizers. There were several in vitro studies reporting that CYP2C19 and CYP3A4 were responsible for the metabolism of 3 PPIs, however, little information is available for their relative contributions on total metabolism, 6-10) that would be adequate to explain that the CYP2C19 genotypedependent pharmacokinetics was more marked for omeprazole than the other two. Herein, to validate further the difference among 3 PPIs in CYP2C19 genotype-dependency on the phenotype, a comparative in vitro study on the metabolism of 3 PPIs was conducted using human liver microsomes and newly developed anti-human CYP antibodies. MATERIALS AND METHODS MaterialsOmeprazole and its two primary metabolites, 5-hydroxyomeprazole and omeprazole sulfone, were obtained from AstraZeneca Ltd. (Osaka, Japan). Lansoprazole and its two primary metabolites, 5-hydroxylansoprazole and lansoprazole sulfone, were obtained from Takeda Pharmaceutical Co. (Osaka, Japan). The internal standard for rabeprazole (IS735), rabeprazole and its two primary metabolites, thioether rabeprazole and rabeprazole sulfone, were obtained from Eisai Co. (Tokyo, Japan). All other chemicals were of reagent grade and obtained commercially. Six lots of human liver microsomes (Table 1) were purchased from KAC Co. Ltd. (Kyoto, Japan). Anti-human CYP antibodies raised against bacterial expressed recombinant human CYP2C19 and CYP3A4 (referred to as anti-CYP2C19 and anti-CYP3A4 antibodies, respectively) were prepared in rabbits according to the method of Kaminsky et al. 11) Cross reactivity of antibodies raised against CYP2C19 and 3A4 were checked by means of ELISA. Anti-CYP2C19 antibody recognized CYP2C19 and slightly cross reacted with CYP2C9, but did not react with CYP1A2, 2D6, 2E1 and 3A4. Under the condition employed in the present study, cross reaction between CYP2C9 and anti-CYP2C19 antibody is minimized. On the other hand, anti-CYP3A4 antibody recognized CYP3A4, but did not react with CYP1A2, 2C9, 2C19, 2D6 and 2E...

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mentioning

confidence: 99%

Different Contribution of CYP2C19 in the in Vitro Metabolism of Three Proton Pump Inhibitors.

Kita

Sakaeda

Baba

et al. 2003

Biological & Pharmaceutical Bulletin

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“…In addition, drug biotransformation is fundamental to generate an active-molecule (M2) from a less (or not) active form (M1) ( Figure 1C). Despite controversies that exist in the literature about the real impact of pharmacogenetics on clinical practice (Padol et al 2006), studies have reported different therapeutic response in patients treated with proton pump inhibitors (Tanigawara et al 1999;Furuta et al 2001;Klotz 2006). These examples illustrate how important PGx is, on a case-by-case basis.…”

Section: Metabolizers Subpopulations a Brief Reviewmentioning

confidence: 99%

Pharmacogenetics and Metabolism: Past, Present and Future

Rios-Santos¹,

Magno²

2012

Topics on Drug Metabolism

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“…Thus, CYP2C19 geno typing may serve as useful new strategy in the choice of an optimal regimen, and this genotype testing may be especially useful in Japan, as the frequency of poor metabolizers among the Japanese is five times greater than that among Caucasians. 74 However, the recent increase in the emergence of antimicrobial-resistant strains of H. pylori may force us to examine the antimicrobial susceptibility in all patients in the near future, in order to achieve an eradication rate with first-line therapy of more than 80%. It would also be imperative to have proper knowledge of the influence of CYP2C19 genetic polymorphism on the treatment efficacy according to various PPIs used alone or in combination with other drugs.…”

Section: Tailor-made Medicine For H Pylori Eradication Therapymentioning

confidence: 99%

Current consensus on the diagnosis and treatment of H. pylori-associated gastroduodenal disease

Suzuki¹,

Masaoka²,

Nomura

et al. 2003

Keio j. med

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Abstract. Helicobacter pylori (H. pylori) is a spiral shaped bacterium that resides in the stomach mucosa. Isolation of H. pylori from the stomach mucosa changed the erstwhile widely held belief that the stomach contains no bacteria and is actually sterile. Once H. pylori is safely ensconced in the mucus, it is able to neutralize the acid in the stomach by elaborating an enzyme called urease. Urease converts urea, of which there is an abundant supply in the stomach (derived from saliva and the gastric juice), into bicarbonate and ammonia, which are strong bases. These bases form a cloud of acid neutralizing chemicals in the vicinity of the organisms, protecting them from the acid in the stomach. This urea hydrolysis reaction is utilized for the diagnosis of H. pylori infection in the urea breath test (UBT) and the rapid urease test (RUT). In Japan, both invasive tests, such as bacterial culture, histopathology and RUT, and non-invasive tests such as UBT and serology are conducted for the diagnosis of H. pylori infection. For confirming the results of eradication therapy, UBT is considered to be the most sensitive and specific. In order to treat H. pylori infection, a new one-week triple therapy regimen (lansoprazole or omeprazole+amoxicillin+clarithromycin) has been approved for use in patients with peptic ulcer disease in Japan. As for H. pylori eradication in the case of other diseases in which the bacterium has been implicated (e.g., chronic atrophic gastritis, gastric MALT lymphoma, gastric cancer, non-ulcer dyspepsia, chronic urticaria, idiopathic thrombocytopenic purpura (ITP)), further basic and clinical investigation is required. (Keio J Med 52 (3): 163-173, September 2003)

show abstract

genotype–related efficacy of omeprazole for the treatment of infection caused by

Cited by 172 publications

References 24 publications

Different Contribution of CYP2C19 in the in Vitro Metabolism of Three Proton Pump Inhibitors.

Different Contribution of CYP2C19 in the in Vitro Metabolism of Three Proton Pump Inhibitors.

Pharmacogenetics and Metabolism: Past, Present and Future

Current consensus on the diagnosis and treatment of H. pylori-associated gastroduodenal disease

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