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Huezo-Diaz, Patricia; Perroud, Nader; Spencer, Edgar P; Smith, Rebecca; Sim, Sarah; Virding, Susanne; Uher, Rudolf; Gunasinghe, Cerisse; Gray, Jo; Campbell, Desmond; Hauser, Joanna; Maier, Wolfgang; Marusic, Andrej; Rietschel, Marcella; Perez, Jorge; Giovannini, Caterina; Mors, Ole; Mendlewicz, Julien; McGuffin, Peter; Farmer, Anne E; Ingelman-Sundberg, Magnus; Craig, Ian W; Aitchison, Katherine J
Journal of psychopharmacology (Oxford), 03/2012, Letnik: 26, Številka: 3Journal Article
In vitro work shows CYP2C19 and CYP2D6 contribute to the metabolism of escitalopram to its primary metabolite, N-desmethylescitalopram. We report the effect of CYP2C19 and CYP2D6 genotypes on steady state morning concentrations of escitalopram and N-desmethylescitalopram and the ratio of this metabolite to the parent drug in 196 adult patients with depression in GENDEP, a clinical pharmacogenomic trial. Subjects who had one CYP2D6 allele associated with intermediate metabolizer phenotype and one associated with poor metabolizer (i.e. IM/PM genotypic category) had a higher mean logarithm escitalopram concentration than CYP2D6 extensive metabolizers (EMs) (p = 0.004). Older age was also associated with higher concentrations of escitalopram. Covarying for CYP2D6 and age, we found those homozygous for the CYP2C19*17 allele associated with ultrarapid metabolizer (UM) phenotype had a significantly lower mean escitalopram concentration (2-fold, p = 0.0001) and a higher mean metabolic ratio (p = 0.0003) than EMs, while those homozygous for alleles conferring the PM phenotype had a higher mean escitalopram concentration than EMs (1.55-fold, p = 0.008). There was a significant overall association between CYP2C19 genotypic category and escitalopram concentration (p = 0.0003; p = 0.0012 Bonferroni corrected). In conclusion, we have demonstrated an association between CYP2C19 genotype, including the CYP2C19*17 allele, and steady state escitalopram concentration.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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