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British Journal of Clinical Pharmacology logoLink to British Journal of Clinical Pharmacology
. 1984 Apr;17(4):470–473. doi: 10.1111/j.1365-2125.1984.tb02374.x

Urinary bile acid and bile alcohol excretion does not reflect the genetic polymorphism of debrisoquine hydroxylation.

G Karlaganis, A Küpfer, R Preisig
PMCID: PMC1463396  PMID: 6721994

Abstract

Excretion of the major urinary bile alcohol 27-nor-5 beta-cholestane-3 alpha, 7 alpha, 12 alpha, 24,25- pentol , and of cholic, chenodeoxycholic, deoxycholic and lithocholic acid was measured in 24 h urine collections of 10 extensive and seven poor metabolizers of debrisoquine. There was no significant difference of the excretion of these cholesterol metabolites between the two groups, indicating that cholesterol hydroxylation to bile alcohols and bile acids is probably not controlled by the same genes responsible for the 'debrisoquine-type' hydroxylation polymorphism.

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Selected References

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