Purine Metabolism in Man—II

Physiology, Pharmacology, and Clinical Aspects

  • Mathias M. Müller
  • Erich Kaiser
  • J. Edwin Seegmiller

Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 76B)

Table of contents

  1. Front Matter
    Pages i-xxii
  2. Renal Handling of Urate

    1. Richard E. Rieselbach
      Pages 1-22
    2. Renal Handling of Urate in Man

      1. B. T. Emmerson, P. J. Ravenscroft, G. Williams
        Pages 23-29
      2. Irving H. Fox, H. B. Stein, S. L. Gershon
        Pages 30-35
      3. F. Matzkies, G. Berg
        Pages 36-40
      4. Peter A. Simkin
        Pages 41-45
      5. T. Gibson, S. F. Hannan, P. J. Hatfield, H. A. Simmonds, J. S. Cameron, C. S. Potter et al.
        Pages 46-55
      6. Herbert S. Diamond, Allen D. Meisel
        Pages 56-62
      7. D. Benjamin, O. Sperling, A. Weinberger, J. Pinkhas, A. de Vries
        Pages 72-76
      8. Bernardo Pinto, Elisabeth Rocha
        Pages 77-80
      9. Bernardo Pinto, Elisabeth Rocha
        Pages 81-85
      10. Bernardo Pinto, Elisabeth Rocha, Francisco J. Ruiz Marcellan
        Pages 86-89
    3. Renal Handling of Urate in Animals

      1. R. Greger, F. Lang, P. Deetjen, F. G. Knox
        Pages 90-99
      2. F. Lang, R. Greger, P. Deetjen, F. G. Knox
        Pages 100-109
      3. R. A. Kramp, F. Diézi-Chométy, R. Lenoir, F. Roch-Ramel
        Pages 117-121
  3. Biochemistry of Purine Transport

About this book


The study of gouty arthritis has provided a common meeting ground for the research interests of both the basic scientist and the clinician. The interest of the chemist in gout began 1776 with the isolation of uric acid from a concretion of the urinary tract by the Swedish chemist SCHEELE. The same substance was subsequently extracted from a gouty tophus by the British chemist WOLLASTONE in 1797 and a half century later the cause of the deposits of sodium urate In such tophi was traced to a hyperuricemia in the serum of gouty patients by the British physician Alfred Baring GARROD who had also received training in the chemical laboratory and was therefore a fore-runner of many of today's clinician-investigators. The recent surge of progress in understanding of some of the causes of gout in terms of specific enzyme defects marks the entrance of the biochemist into this field of investigation. The identification of the first primary defect of purine metabolism associated with over-production of uric acid, a severe or partial deficiency of the enzyme hypoxanthine-guanine phospho­ ribosyl transferase was achieved less than a decade ago. The knowledge of the mechanism of purine over-production that it generated led shortly to the identification of families carrying a dominantly (possibly X-linked) inherited increase in the activity of the enzyme phosphoribosylpyrophosphate synthetase as a cause of purine over-production. Yet this is only a start as these two types of enzyme defects account for less than five per cent of gouty patients.


Purine enzyme enzymes metabolism research

Editors and affiliations

  • Mathias M. Müller
    • 1
  • Erich Kaiser
    • 1
  • J. Edwin Seegmiller
    • 2
  1. 1.University of ViennaViennaAustria
  2. 2.University of CaliforniaSan Diego, La JollaUSA

Bibliographic information

  • DOI https://doi.org/10.1007/978-1-4684-3285-5
  • Copyright Information Springer-Verlag US 1977
  • Publisher Name Springer, Boston, MA
  • eBook Packages Springer Book Archive
  • Print ISBN 978-1-4684-3287-9
  • Online ISBN 978-1-4684-3285-5
  • Series Print ISSN 0065-2598
  • About this book