Hf. Alhadidi et al., METOPROLOL ALPHA-HYDROXYLATION IS A POOR PROBE FOR DEBRIZOQUINE OXIDATION (CYP2D6) POLYMORPHISM IN JORDANIANS, European Journal of Clinical Pharmacology, 47(4), 1994, pp. 311-314
The frequency distribution of the 8-h urinary ratio of log metoprolol/
alpha-hydroxymetoprolol was assessed in 65 healthy, unrelated Jordania
n volunteers. There was no apparent bimodality in the frequency distri
bution of this ratio among the subjects studied. The frequency of the
poor metabolizer phenotype of metoprolol alpha-hydroxylation was 1.5 %
(one subject). There was a significant correlation (r = 0.61, P < 0.0
5, n = 39) between the log metoprolol/alpha-hydroxymetoprolol and the
log debrisoquine/4-hydroxydebrisoquine ratios. However, the frequency
of poor metabolizer status of debrisoquine among the 39 subjects was 7
.7 % (three subjects). Only one of the poor metabolizers of debrisoqui
ne was also a poor metabolizer of metoprolol alpha-hydroxylation. Thes
e findings indicate that metoprolol alpha-hydroxylation by CYP2D6 repr
esents a poor probe for studying debrisoquine polymorphism in Jordania
ns.