Effect of the CYP2D6 genotype on prolactin concentration in schizophrenic patients treated with haloperidol
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K. Otani | A. Suzuki | S. Kaneko | Y. Inoue | T. Kondo | N. Tokinaga | K. Mihara | N. Yasui‐Furukori
[1] K. Otani,et al. Prolactin response to nemonapride, a selective antagonist for D2 like dopamine receptors, in schizophrenic patients in relation to Taq1A polymorphism of DRD2 gene , 2000, Psychopharmacology.
[2] S. Ulrich,et al. Reduced haloperidol does not interfere with the antipsychotic activity of haloperidol in the treatment of acute schizophrenia. , 1999, International clinical psychopharmacology.
[3] K. Otani,et al. Effects of the CYP2D6*10 allele on the steady‐state plasma concentrations of haloperidol and reduced haloperidol in Japanese patients with schizophrenia , 1999, Clinical pharmacology and therapeutics.
[4] R. Petty. Prolactin and antipsychotic medications: mechanism of action , 1999, Schizophrenia Research.
[5] L. Farde,et al. Plasma prolactin and central D2 receptor occupancy in antipsychotic drug-treated patients. , 1998, Journal of clinical psychopharmacology.
[6] K. Otani,et al. Prolactin response to bromperidol treatment in schizophrenic patients. , 1998, Pharmacology & toxicology.
[7] K. Otani,et al. Effects of the CYP2D6 genotype on the steady-state plasma concentrations of haloperidol and reduced haloperidol in Japanese schizophrenic patients. , 1997, Pharmacogenetics.
[8] L. Bertilsson,et al. Polymorphic Drug Oxidation , 1996 .
[9] O. Andreassen,et al. Detection of the poor metabolizer-associated CYP2D6(D) gene deletion allele by long-PCR technology. , 1995, Pharmacogenetics.
[10] M. Ingelman-Sundberg,et al. Genetic analysis of the Chinese cytochrome P4502D locus: characterization of variant CYP2D6 genes present in subjects with diminished capacity for debrisoquine hydroxylation. , 1994, Molecular pharmacology.
[11] M. W. Tsang,et al. Metabolism of haloperidol: clinical implications and unanswered questions. , 1994, Journal of clinical psychopharmacology.
[12] K. Otani,et al. Prolactin response to zotepine in schizophrenic patients , 1993 .
[13] L. Bertilsson,et al. Haloperidol disposition is dependent on the debrisoquine hydroxylation phenotype: increased plasma levels of the reduced metabolite in poor metabolizers. , 1992, Therapeutic drug monitoring.
[14] C. Alm,et al. Haloperidol disposition is dependent on debrisoquine hydroxylation phenotype. , 1992, Therapeutic drug monitoring.
[15] S. Marder,et al. Serum prolactin as a correlate of clinical response to haloperidol. , 1991, Journal of clinical psychopharmacology.
[16] U. Meyer,et al. Genotyping of poor metabolisers of debrisoquine by allele-specific PCR amplification , 1990, The Lancet.
[17] W. Bowen,et al. Metabolites of haloperidol display preferential activity at sigma receptors compared to dopamine D-2 receptors. , 1990, European journal of pharmacology.
[18] Y. Ohkura,et al. Determination of bromperidol in serum by automated column-switching high-performance liquid chromatography. , 1989, Journal of chromatography.
[19] H. Meltzer,et al. Psychopharmacology : the third generation of progress , 1987 .
[20] P. Jatlow,et al. Ratio of serum prolactin to haloperidol and early clinical outcome in acute psychosis. , 1984, The American journal of psychiatry.
[21] R. Lu,et al. Prolactin response to single and multiple doses of haloperidol in schizophrenic patients , 1984, Psychiatry Research.
[22] R. Rubin,et al. Serum haloperidol determinations in psychiatric patients. Comparison of methods and correlation with serum prolactin level. , 1980, Archives of general psychiatry.