Deficient metabolism of debrisoquine and sparteine

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Abstract
Genetic deficiencies of alicyclic hydroxylation of debrisoquine and of sparteine oxidation are independently discovered entities, each of clinical significance in its sphere. Evidence indicates that these 2 deficiencies have the same cause. Previous investigation of one of the affected subjects had revealed normal oxidative metabolism of amobarbital and antipyrine in terms of both metabolic rates and urinary metabolite patterns. The genetic defect in the metabolism of sparteine and debrisoquine is not a generalized deficiency of drug oxidation or of the cytochrome P450 system.