The genetic polymorphism of debrisoquine/sparteine metabolism - clinical aspects. Pharmacokinetics of the selective serotonin reuptake inhibitor paroxetine: nonlinearity and relation to the sparteine oxidation polymorphism.Kirchheiner J, Henckel HB, Meineke I, Roots I, Brockmöller J . The CYP2C19 enzyme polymorphism.Schwab M, Schaeffeler E, Klotz U, Treiber G . 625–648.Eichelbaum M, Spannbrucker N, Steincke B and Dengler HJ (1979). Epub 2006 Aug 19.Ishizu S, Hashida C, Hanaoka T, Maeda K, Ohishi Y.Jpn J Cancer Res. Influence of CYP2D6 activity on the disposition and cardiovascular toxicity of the antidepressant agent venlafaxine in humans.Chen S, Chou WH, Blouin RA, Mao Z, Humphries LL, Meek QC,Kirchheiner J, Brosen K, Dahl ML, Gram LF, Kasper S, Roots I.Lennard MS, Silas JH, Freestone S, Trevethick J . The metabolism of isoniazid, its implications in therapeutic use. Mephenytoin hydroxylation in the Cuna Indians of Panama.Iselius, L. and Price Evans, D.A.P. Pharmacogenetics of the proton pump inhibitors: a systematic review.Fuhr U, Jetter A . Relationship between fluvoxamine pharmacokinetics and CYP2D6/CYP2C19 phenotype polymorphisms.Carrillo JA, Dahl ML, Svensson JO, Alm C, Rodriguez I, Bertilsson L . Q.Sanz, E.J., Villen, T., Alm, C. & Bertilsson, L. (1989). Some drugs used for relief of these ailments are metabolized with participation of genetically polymorphic DMEs including CYP2D6, CYP2C9, CYP2C19, thiopurine-.Despite its profound progress, modern pharmacotherapy still faces many challenges such as adverse drug reactions, sometimes serious or even lethal, and nonresponse to standard therapy. Since variation in drug concentrations resulting from respective genetic polymorphisms in DMEs could be directly implemented into dose adjustments, genotyping for DMEs seems to be the closest to incorporation into clinical practice.The importance of genetic variants of DMEs to explain interindividual differences in drug concentrations and corresponding pharmacodynamic effects has been recognized about 50 years ago.The objective of this article is to critically review the data on genetic polymorphisms of DMEs with emphasis on clinical relevance and the level of evidence, in order to define situations where genotyping or phenotyping might be beneficial for drug safety or therapeutic outcome. Part of.These keywords were added by machine and not by the authors. & Mc Kusick, V.A. Sulfadimidine acetylation test for classification of patients as slow or rapid inactivators of isoniazide.Robitzek, E.H., Selikoff, I.J. Increased incidence of isoniazid hepatitis in rapid acetylators: Possible relation to hydrazine metabolites.Musch, E., Eichelbaum, M., Wang, J.K.V., Sassen, W., Castro-Parra, M. ac Dengler, H.J. 609–623.Price Evans DA (1992). These polymorphisms have provided useful tools for the study of the relationship between genetically determined differences in the activity of drug metabolizing enzymes and the risk of adverse drug reactions and certain types of chemically induced diseases and cancers.Over 10 million scientific documents at your fingertips,© 2020 Springer Nature Switzerland AG. Human polymorphic enzymes and the global distribution of major variant alleles Allele frequency (%) Consequence No. (1977). Genetic polymorphisms of drug metabolism. The frequency of the PM phenotype differs according to geographical distribution (Caucasian populations 2–5%, Chinese/Japanese populations 15–23%).Whether or not a deficient pathway in the metabolism of certain drugs has clinical relevance obviously depends on the relative importance of the affected pathway to the overall elimination of the compound. Characterization of cDNAs, mRNAs and proteins related to human liver microsomal cytochrome P-450 S-mephenytoin 4-hydroxylase.Gonzalez, F.J. (1989). The possible complications in therapy with oral anticoagulants involve severe bleedings or lack of efficacy resulting from, respectively, over- and underanticoagulation. Human debrisoquine 4-hydroxylase (P450IID1): cDNA and deduced amino acid sequence and assignment of the CYP2D locus to chromosome 22.Gonzalez, F.J., Skoda, R.C., Kimura, S., Umeno, M., Zanger, U.M., Nebert, D.W., Gelboin, H.V., Hardwick, J.P. and Meyer, U.A. Polymorphic acetylation and aminopyrine demethylation in Gilbert’s syndrome.Price Evans, D.A. (1987). Part of.These keywords were added by machine and not by the authors. ), pp. Inheritance of phenytoin hypometabolism: a kinetic study of one family.Wilkinson GR (1989).Pharmacogenetic factors responsible for variability in drug disposition. The genetic polymorphism of debrisoquine/sparteine - clinical aspects.Eichelbaum, M., Spannbrucker, N., Steincke, B. and Dengler, H.J. Stereoselective disposition of carvedilol in man after intravenous and oral administration of the racemic compound.Zhou HH, Wood AJJ . In addition, we compared the fluvastatin pharmacokinetics differences between extended-release (ER) 80 mg tablet and immediate-release (IR) 40 mg capsule in terms of drug metabolism enzyme and transporter genetic polymorphisms. New,Dr. Further work has established genetic … The role of cytochrome P450 2D6 in the metabolism of moclobemide.Gram LF, Guentert TW, Grange S, Vistisen K, Brøsen K . Variants leading to reduced or increased enzymatic activity as compared to the wild-type alleles have been identified. Partial purification and properties of the isoniazid transacetylase in human liver: Its relationship to the acetylation of p-amino-salicylic acid.Kaisary, A., Smith, P., Jaczq, E., McAllister, B., Wilkinson,G.R., Ray, W.A. Genetic polymorphisms also exist with respect to drug oxidation and a close relationship has been shown to exist between an individual’s ability to oxidise debrisoquine and sparteine and numerous drugs have been identified whose metabolism is affected by this polymorphism (5–10% PM in Caucasian populations but 0–2% in Japanese/Chinese populations). and Guengerich, F.P. (1987). In: Kalow W (ed. and Guengerich, F.P. Such differences mainly translate into differences in susceptibility for drug toxicity. Xenobiotic and endobiotic inhibitors of cytochrome P-450dbl function, the target of the debrisoquine/sparteine type polymorphism.Ged, C., Umbenauer, D.R., Bellew, T.M., Bork, R.W., Srivastava, P.K., Shinriki, N., Lloyd,R.S.

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