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Deficient Benzbromarone Elimination from Plasma: Evidence for a New Genetically Determined Polymorphism with an Autosomal Recessive Inheritance

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Purine and Pyrimidine Metabolism in Man VII

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 309A))

Abstract

Benzbromarone is one of the three most important uricosuric drugs and widely used in Europe. Initially it was reported to be debrominated to bromobenzarone and benzarone, as shown by Yü (1976). Recently Ingeborg Walter-Sack from Heidelberg and her coworkers (Walter-Sack et al 1987; Walter-Sack et al 1990b) could show that hydroxilation is the primary metabolic pathway. When the elimination of benzbromarone was determined by measuring plasma concentration in healthy subjects one unusual case was found. In this individual plasma concentration 12 hours after oral administration was ten times higher than in the others. 24 hours after drug application this person had still a measurable benzbromarone plasma concentration, which was higher than the 12 hours plasma concentration of the others (Walter-Sack et al 1988). The elevated 24 hours plasma concentration was thought to be the characteristic metabolic feature of deficient benzbromarone elimination.

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© 1991 Springer Science+Business Media New York

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Gresser, U., Adjan, M., Zöllner, N. (1991). Deficient Benzbromarone Elimination from Plasma: Evidence for a New Genetically Determined Polymorphism with an Autosomal Recessive Inheritance. In: Harkness, R.A., Elion, G.B., Zöllner, N. (eds) Purine and Pyrimidine Metabolism in Man VII. Advances in Experimental Medicine and Biology, vol 309A. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-2638-8_35

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  • DOI: https://doi.org/10.1007/978-1-4899-2638-8_35

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4899-2640-1

  • Online ISBN: 978-1-4899-2638-8

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