Sulphasalazine (salicyl-azo-sulphapyridine) was ingested by 27 healthy subjects for five days at a dosage of 4 g daily. The acetylator phenotype of each subject had been established previously. The serum concentrations of the parent drug and its sulphapyridine-metabolites were determined and the adverse effects were recorded. There was no correlation between the serum concentrations of sulphasalazine and the adverse effects. The slow acetylators obtained enhancement of serum concentrations of sulphapyridine earlier than the rapid acetylators. They also reported adverse effects earlier and of more pronounced nature than the rapid acetylators. The data as a whole suggest that the adverse effects observed were caused by the metabolite sulphapyridine and that they are influenced by the polymorphic acetylation.
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