METOPROLOL ALPHA-HYDROXYLATION IS A POOR PROBE FOR DEBRIZOQUINE OXIDATION (CYP2D6) POLYMORPHISM IN JORDANIANS

Citation
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
Citations number
17
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
00316970
Volume
47
Issue
4
Year of publication
1994
Pages
311 - 314
Database
ISI
SICI code
0031-6970(1994)47:4<311:MAIAPP>2.0.ZU;2-S
Abstract
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.