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J Med Genet. 1980 April; 17(2): 102–105.
PMCID: PMC1048511

A family and population study of the genetic polymorphism of debrisoquine oxidation in a white British population.


A population survey of 258 unrelated white British subjects showed a polymorphism for the 4-oxidation of debrisoquine. "Extensive metabolisers" (EM) and "poor metabolisers" (PM) are recognisable, 8.9% of the population being PM. Nine pedigrees ascertained through PM probands show that the PM phenotype is an autosomal Mendelian recessive character. The EM phenotype is dominant and the degree of dominance has been estimated at 30%. PM subjects are more prone to hypotension during debrisoquine therapy. The alleles controlling this polymorphism appear to control the oxidation of other drugs.

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Selected References

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  • Mahgoub A, Idle JR, Dring LG, Lancaster R, Smith RL. Polymorphic hydroxylation of Debrisoquine in man. Lancet. 1977 Sep 17;2(8038):584–586. [PubMed]
  • Idle JR, Mahgoub A, Angelo MM, Dring LG, Lancaster R, Smith RL. The metabolism of [14C]-debrisoquine in man. Br J Clin Pharmacol. 1979 Mar;7(3):257–266. [PubMed]
  • Sloan TP, Mahgoub A, Lancaster R, Idle JR, Smith RL. Polymorphism of carbon oxidation of drugs and clinical implications. Br Med J. 1978 Sep 2;2(6138):655–657. [PMC free article] [PubMed]
  • Kitchen I, Tremblay J, André J, Dring LG, Idle JR, Smith RL, Williams RT. Interindividual and interspecies variation in the metabolism of the hallucinogen 4-methoxyamphetamine. Xenobiotica. 1979 Jul;9(7):397–404. [PubMed]

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