Key result
CYP2D6 genotypes predicting lower enzyme activity were associated with higher plasma concentrations of metoprolol, demonstrating a 100-fold variation in concentrations among cardiovascular patients.
Why the study?
Does CYP2D6 genetic polymorphism influence steady-state plasma concentrations and apparent oral clearance of metoprolol in cardiovascular patients?
Observational (n=91)
Does CYP2D6 genetic polymorphism influence steady-state plasma concentrations and apparent oral clearance of metoprolol in cardiovascular patients?
CYP2D6 genetic polymorphisms significantly influence metoprolol plasma concentrations and clearance, suggesting pharmacogenetic testing could guide individualized dosing.
Leaves open CYP2D6-guided metoprolol dosing in practice; extends genotype-concentration associations from healthy volunteers to cardiovascular patients.
BACKGROUND AND OBJECTIVE: CYP2D6 polymorphisms are well described in normal populations but there are few data on its clinical significance. We therefore investigated the influence of CYP2D6 polymorphism on steady-state plasma concentrations and apparent oral clearance of metoprolol in patients with cardiovascular diseases. METHODS: Ninety-one patients on metoprolol were recruited. Plasma concentrations of metoprolol and alpha-hydroxy metoprolol were measured at 4-h post-dose. CYP2D6 genotyping (*1, *3, *4, *5, *9, *8, *10, *17 and duplication) were performed on the DNA extracted. Ratio of plasma concentrations of metoprolol and alpha-hydroxy metoprolol and the apparent oral clearance of metoprolol were calculated. The influences of CYP2D6 genotypes were investigated. RESULTS: A 100-fold variation was noted for both plasma concentrations of metoprolol and alpha-hydroxy metoprolol. There was a weak correlation between the total daily doses and plasma concentrations of both. Plasma concentrations were found to be higher in patients with genotypes that predicted lower enzyme activity. One patient homozygous for CYP2D6*4 had the highest metoprolol concentration per unit dose. With an antimode of 10. Two patients were identified as poor metabolizers (PMs) (2.1%; 95% CI: 2.9). The PMs who had a plasma metabolic ratio (pMR) of 37.8 was homozygous CYP2D6*4 whereas the other with pMR 14.5 was genotyped CYP2D6 *4/*10. There was a 36-fold difference between the highest and lowest clearance values. Large overlaps in the clearance values were noted between most of the genotypes. CONCLUSIONS: Our data suggest that pharmacogenetic measures could be used to design a more individualized metoprolol dosage regimen for patients.
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Ismail et al. (2006) conducted an observational in cardiovascular diseases (n=91). CYP2D6 polymorphism was evaluated on steady-state plasma concentrations and apparent oral clearance of metoprolol. CYP2D6 genotypes predicting lower enzyme activity were associated with higher plasma concentrations of metoprolol, demonstrating a 100-fold variation in concentrations among cardiovascular patients.
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