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.