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Hydroxylation polymorphism of debrisoquine hydroxylase (CYP2D6) in patients with schizophrenia in Norway and Denmark
Author(s) -
Dahl Alv A.,
Løwert Anette,
Asserson Sigurd,
Bjarking Lennart,
Berglund Johan,
Kristensen Flemming,
Norum Dag,
Tønseth Sverre,
Bayer Lotte,
Mæhlum Eli
Publication year - 1998
Publication title -
human psychopharmacology: clinical and experimental
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.461
H-Index - 78
eISSN - 1099-1077
pISSN - 0885-6222
DOI - 10.1002/(sici)1099-1077(1998100)13:7<509::aid-hup32>3.0.co;2-1
Subject(s) - debrisoquine , cyp2d6 , danish , hydroxylation , sparteine , genotyping , pharmacogenetics , norwegian , isozyme , medicine , haloperidol , polymorphism (computer science) , pharmacology , chemistry , genetics , endocrinology , allele , biology , biochemistry , enzyme , metabolism , dopamine , genotype , cytochrome p450 , stereochemistry , gene , linguistics , philosophy
The isozyme debrisoquine hydroxylase (CYP2D6) is central for the elimination of neuroleptic drugs. The capacity to hydroxylate debrisoquine is currently examined by genotyping of the isozyme. Approximately 7% of Europeans have a reduced capacity to hydroxylate debrisoquine, and they are defined as poor metabolizers. Two studies of small samples of well‐defined patients with schizophrenia have shown that 6·5–6·6% were poor metabolizers, which is close to the rate in psychic normals. We found a total rate of 3·9% of poor metabolizers in a big sample ( N =509) of patients with schizophrenia. The rate in the Danish subsample ( N =221) was 4·5%, and in the Norwegian subsample ( N =288) the rate was 3·5%. Our results indicate that the true rate of poor metabolizers among patient's with schizophrenia is still to be determined. © 1998 John Wiley & Sons, Ltd.