Metoprolol α-hydroxylation is a poor probe for debrizoquine oxidation (CYP2D6) polymorphism in Jordanians
✍ Scribed by H. F. Al-Hadidi; Y. M. Irshaid; N. M. Rawashdeh
- Publisher
- Springer
- Year
- 1994
- Tongue
- English
- Weight
- 358 KB
- Volume
- 47
- Category
- Article
- ISSN
- 0031-6970
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✦ Synopsis
The frequency distribution of the 8-h urinary ratio of log metoprolol/ct-hydroxymetoprolol was assessed in 65 healthy, unrelated Jordanian volunteers.
There was no apparent bimodality in the frequency distribution of this ratio among the subjects studied. The frequency of the poor metabolizer phenotype of metoprolol a-hydroxylation was 1.5 % (one subject). There was a significant correlation (r = 0.61, P < 0.05, n = 39) between the log metoprolol/a-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 debrisoquine was also a poor metabolizer of metoprolol a-hydroxylation.
These findings indicate that metoprolol ~-hydroxylation by CYP2D6 represents a poor probe for studying debrisoquine polymorphism in Jordanians.