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Article: Failure to respond to treatment with typical antipsychotics is not associated with CYP2D6 ultrarapid hydroxylation

TitleFailure to respond to treatment with typical antipsychotics is not associated with CYP2D6 ultrarapid hydroxylation
Authors
Issue Date1999
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/BJCP
Citation
British Journal Of Clinical Pharmacology, 1999, v. 48 n. 3, p. 388-394 How to Cite?
AbstractAims. To investigate whether or not there is a correlation between failure to respond to typical antipsychotics and CYP2D6 ultrarapid metaboliser status. Methods. CYP2D6 phenotype (metaboliser status) was assigned following genotyping for gene duplication, as well as for the CYP2D6*3, CYP2D6*4, and CYP2D6*5 null alleles in 235 treatment-refractory patients and 73 nonrefractory patients. Results. Four (1.7%) of the 235 treatment-refractory subjects were positive on the duplication assay, but, of these, two were found to represent duplications of a null allele (CYP2D6*4), therefore leaving only two (0.85%) positive for duplication of a wild type allele (ultrarapid metabolisers). Three (4.1%) of the nonrefractory subjects had a genotype consistent with ultrarapid metaboliser status. Fisher's exact test gave a two-tailed P value of 0.091, i.e. a trend towards an excess of ultrarapid metabolisers in the nonrefractory group, which was in the opposite direction to that predicted by our hypothesis. Conclusions. Although the results show a trend towards an excess of ultrarapid metabolisers in the nonrefractory group, the percentages in the two groups of patients are both within the range for ultrarapid metabolisers in Caucasian populations. Our data are not consistent with ultrarapid metaboliser status being a major cause of failure to respond to typical antipsychotics.
Persistent Identifierhttp://hdl.handle.net/10722/175800
ISSN
2015 Impact Factor: 3.83
2015 SCImago Journal Rankings: 1.486
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorAitchison, KJen_US
dc.contributor.authorMunro, Jen_US
dc.contributor.authorWright, Pen_US
dc.contributor.authorSmith, Sen_US
dc.contributor.authorMakoff, AJen_US
dc.contributor.authorSachse, Cen_US
dc.contributor.authorSham, PCen_US
dc.contributor.authorMurray, RMen_US
dc.contributor.authorCollier, DAen_US
dc.contributor.authorKerwin, RWen_US
dc.date.accessioned2012-11-26T09:01:24Z-
dc.date.available2012-11-26T09:01:24Z-
dc.date.issued1999en_US
dc.identifier.citationBritish Journal Of Clinical Pharmacology, 1999, v. 48 n. 3, p. 388-394en_US
dc.identifier.issn0306-5251en_US
dc.identifier.urihttp://hdl.handle.net/10722/175800-
dc.description.abstractAims. To investigate whether or not there is a correlation between failure to respond to typical antipsychotics and CYP2D6 ultrarapid metaboliser status. Methods. CYP2D6 phenotype (metaboliser status) was assigned following genotyping for gene duplication, as well as for the CYP2D6*3, CYP2D6*4, and CYP2D6*5 null alleles in 235 treatment-refractory patients and 73 nonrefractory patients. Results. Four (1.7%) of the 235 treatment-refractory subjects were positive on the duplication assay, but, of these, two were found to represent duplications of a null allele (CYP2D6*4), therefore leaving only two (0.85%) positive for duplication of a wild type allele (ultrarapid metabolisers). Three (4.1%) of the nonrefractory subjects had a genotype consistent with ultrarapid metaboliser status. Fisher's exact test gave a two-tailed P value of 0.091, i.e. a trend towards an excess of ultrarapid metabolisers in the nonrefractory group, which was in the opposite direction to that predicted by our hypothesis. Conclusions. Although the results show a trend towards an excess of ultrarapid metabolisers in the nonrefractory group, the percentages in the two groups of patients are both within the range for ultrarapid metabolisers in Caucasian populations. Our data are not consistent with ultrarapid metaboliser status being a major cause of failure to respond to typical antipsychotics.en_US
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/BJCPen_US
dc.relation.ispartofBritish Journal of Clinical Pharmacologyen_US
dc.subject.meshAllelesen_US
dc.subject.meshAntipsychotic Agents - Metabolism - Therapeutic Useen_US
dc.subject.meshCytochrome P-450 Cyp2d6 - Genetics - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshHydroxylationen_US
dc.subject.meshSchizophrenia - Drug Therapy - Enzymologyen_US
dc.subject.meshTreatment Failureen_US
dc.titleFailure to respond to treatment with typical antipsychotics is not associated with CYP2D6 ultrarapid hydroxylationen_US
dc.typeArticleen_US
dc.identifier.emailSham, PC: pcsham@hku.hken_US
dc.identifier.authoritySham, PC=rp00459en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1046/j.1365-2125.1999.00006.xen_US
dc.identifier.pmid10510151-
dc.identifier.scopuseid_2-s2.0-0032821401en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032821401&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume48en_US
dc.identifier.issue3en_US
dc.identifier.spage388en_US
dc.identifier.epage394en_US
dc.identifier.isiWOS:000082808900016-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridAitchison, KJ=7003415672en_US
dc.identifier.scopusauthoridMunro, J=7102726057en_US
dc.identifier.scopusauthoridWright, P=7404316244en_US
dc.identifier.scopusauthoridSmith, S=8534162000en_US
dc.identifier.scopusauthoridMakoff, AJ=7006063526en_US
dc.identifier.scopusauthoridSachse, C=7003792226en_US
dc.identifier.scopusauthoridSham, PC=34573429300en_US
dc.identifier.scopusauthoridMurray, RM=35406239400en_US
dc.identifier.scopusauthoridCollier, DA=26642980600en_US
dc.identifier.scopusauthoridKerwin, RW=7102904567en_US

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