PURPOSE: Cytochrome P450 2D6 (CYP2D6) genotypes and the dextromethorphan/dextrorphan (DXM/DXT) metabolic ratio (MR), which is a marker of CYP2D6 activity, were studied in 118 unrelated healthy Ecuadorians. METHODS: Genotyping of CYP2D6 was performed by amplification of entire CYP2D6 gene by XL-PCR for CYP2D6*5 and multiplication alleles and by real time-PCR for CYP2D6 *2, *3, *4, *6, *10, *17, *29, *35, *41, and copy number. The plasma levels of DXM and its metabolite DXT were determined on a high-performance liquid chromatography-UV system. RESULTS: The proportions of non-functional alleles were 0.4, 10.6, 0.8, 2.1, and 0% for CYP2D6*3, *4, *4 × N, *5, and *6, respectively. Genotypically, only one of the subjects (0.9%) was homozygous for two inactive alleles and phenotypically classified as a poor metabolizer (PM). The MRs (mean ± standard deviation) corresponding to "activity scores" of 0, 0.5, 1, 1.5, 2, and 2.5 were 10.57 (n = 1), 1.63 ± 0.35 (n = 2), 1.16 ± 0.74 (n = 29), 1.00 ± 0.47 (n = 8), 1.24 ± 0.82 (n = 76), and 1.30 ± 0.32 (n = 2), respectively. CONCLUSIONS: Our data suggest that only 1% of subjects of this Ecuadorian population were PMs and that none were phenotypically ultrarapid metabolizers, which is in agreement with previous findings in other Amerindian populations.
PURPOSE:Cytochrome P450 2D6 (CYP2D6) genotypes and the dextromethorphan/dextrorphan (DXM/DXT) metabolic ratio (MR), which is a marker of CYP2D6 activity, were studied in 118 unrelated healthy Ecuadorians. METHODS: Genotyping of CYP2D6 was performed by amplification of entire CYP2D6 gene by XL-PCR for CYP2D6*5 and multiplication alleles and by real time-PCR for CYP2D6 *2, *3, *4, *6, *10, *17, *29, *35, *41, and copy number. The plasma levels of DXM and its metabolite DXT were determined on a high-performance liquid chromatography-UV system. RESULTS: The proportions of non-functional alleles were 0.4, 10.6, 0.8, 2.1, and 0% for CYP2D6*3, *4, *4 × N, *5, and *6, respectively. Genotypically, only one of the subjects (0.9%) was homozygous for two inactive alleles and phenotypically classified as a poor metabolizer (PM). The MRs (mean ± standard deviation) corresponding to "activity scores" of 0, 0.5, 1, 1.5, 2, and 2.5 were 10.57 (n = 1), 1.63 ± 0.35 (n = 2), 1.16 ± 0.74 (n = 29), 1.00 ± 0.47 (n = 8), 1.24 ± 0.82 (n = 76), and 1.30 ± 0.32 (n = 2), respectively. CONCLUSIONS: Our data suggest that only 1% of subjects of this Ecuadorian population were PMs and that none were phenotypically ultrarapid metabolizers, which is in agreement with previous findings in other Amerindian populations.
Authors: W J Tamminga; J Wemer; B Oosterhuis; J P Brakenhoff; M G Gerrits; R A de Zeeuw; L F de Leij; J H Jonkman Journal: Eur J Clin Pharmacol Date: 2001-05 Impact factor: 2.953
Authors: M E G Naranjo; F de Andrés; A Delgado; J Cobaleda; E M Peñas-Lledó; A LLerena Journal: Pharmacogenomics J Date: 2016-06-07 Impact factor: 3.550