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

TLDR

A survey of 258 unrelated white British subjects revealed a polymorphism in debrisoquine 4‑oxidation. The study identified two metabolizer phenotypes—extensive (EM) and poor (PM)—with 8.9% of subjects as PM; PM inheritance is autosomal recessive, EM is dominant with ~30% dominance, PM subjects are more prone to hypotension during debrisoquine therapy, and the polymorphic alleles also influence the oxidation of other drugs.

Abstract

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.