Skip to main content
SpringerLink
Log in

Clinical and biochemical aspects of uric acid overproduction

  • Published:
Pharmacy World and Science Aims and scope Submit manuscript

Abstract

Purine nucleotides are synthesized and degraded through a regulated series of reactions which end in the formation of uric acid. Increased uric acid synthesis may be the result of two major pathophysiological disorders: increasedde novo purine synthesis and enhanced purine nucleotide degradation, both of which may be the result of an increased or decreased enzyme activity. In addition, some conditions and disorders associated with uric acid overproduction have been recognized as the result of increased ATP degradation or decreased synthesis of ATP. The clinical manifestations of the diseases leading to excess uric acid synthesis are heterogenous, but symptoms related to uric acid overproduction are always secondary to the precipitation of crystals in soft tissues, joints, and the kidney excretory system. In clinical practice, serum urate concentration and urinary uric acid excretion arc used to assess uric acid synthesis, taking into account that a purine-rich diet can be a confounding variable. Quantification of uric acid precursors, such as adenosine, inosine, guanosine, hypoxanthine, and xanthine, in biological fluids and intracellular nucleotides has provided further insight into the metabolic disturbances underlying disorders associated with uric acid overproduction. Additional studies are necessary to define precisely the metabolic derangement in idiopathic uric acid overproduction and to assess fully the consequences of increased purine nucleotide degradation, such as free-radical formation, increased adenosine synthesis, and reduced synthesis of signal transducers.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Similar content being viewed by others

References

  1. Palella TD, Fox IH. Hyperuricemia and gout. In: Scriver CR, Beaudet AL, Sly WS, Valle D, editors. The metabolic basis of inherited disease. 6th ed. New York: McGraw-Hill, 1989:965–1006.

    Google Scholar 

  2. Holmes EW, Wyngaarden JB, Kelley WN. Human glutamine phosphoribosylpyrophosphate aminotransferase: two molecular forms interconvertible by purine ribonucleotides and phosphoribosylpyrophosphate. J Biol Chem 1973;248:6035–40.

    PubMed  Google Scholar 

  3. Hers H-G, Van den Berghe G. Enzyme defect in primary gout. Lancet 1979;1:585–6.

    PubMed  Google Scholar 

  4. Emmerson BT. Identification of the causes of persistent hyperuricemia. Lancet 1992;337:1461–3.

    Google Scholar 

  5. Kelley WN, Fox IH, Palella TD. Gout and related disorders of purine metabolism. In: Kelley WN, Harris ED Jr, Ruddy S, Sledge CB, editors. Textbook of rheumatology. Philadelphia: WB Saunders Co, 1989:1395–448.

    Google Scholar 

  6. Edwards NL, Recker D, Fox IH. Overproduction of uric acid in hypoxanthine-guanine phosphoribosyltransferase deficiency. Contribution by impaired purine salvage. J Clin Invest 1979;63:922–30.

    PubMed  Google Scholar 

  7. Puig JG, Mateos FA, Jiménez ML, Ramos TH. Renal excretion of hypoxanthine and xanthine in primary gout. Am J Med 1988;85:533–7.

    PubMed  Google Scholar 

  8. Kaufman JM, Greene ML, Seegmiller JE. Urine uric acid to creatinine ratio: a screening test for inherited disorders of purine metabolism. J Pediatr 1968;73:583–92.

    PubMed  Google Scholar 

  9. Sperling O, Eilam G, Persky-Brosh S, de Vries A. Accelerated erythrocyte 5-phosphoribosyl-1-pyrophosphate synthesis. A familial abnormality associated with excessive uric acid production and gout. Biochem Med 1972;6:310–6.

    PubMed  Google Scholar 

  10. Becker MA, Yen RCK, Otkin P, Goss SJ, Seegmiller JE, Bakay B. Regional localization of the gene for human phosphoribosylpyrophosphate synthetase on the X-chromosome. Science 1979;20:1016–9.

    Google Scholar 

  11. Becker MA. Phosphoribosylpyrophosphate synthetase superactivity: detection, characterization of underlying defects and treatment. Adv Exp Med Biol 1984;165A:91–6.

    Google Scholar 

  12. Becker MA, Losman MJ, Rosenberg AL, Mehlman I, Levinson DJ, Holmes EW. Phosphoribosylpyrophosphate synthetase superactivity. Arthritis Rheum 1986;29:880–8.

    PubMed  Google Scholar 

  13. Nyhan WL, James JA, Teberg AJ, Sweetman L, Nelson LG. A new disorder of purine metabolism with behavioral manifestations. J Pediatr 1969;74:20–7.

    PubMed  Google Scholar 

  14. Rosenberg AL, Bergstrom L, Troost BT, Bartholomew BA. Hyperuricemia and neurologic deficits. N Engl J Med 1970;282:992–7.

    PubMed  Google Scholar 

  15. Becker MA, Raivio KO, Bakay B, Adams WB, Nyhan WL. Variant human phosphoribosylpyrophosphate synthetase altered in regulatory and catalytic functions. J Clin Invest 1980;65:109–20.

    PubMed  Google Scholar 

  16. Simmonds HA, Webster DR, Wilson J, Lingham S. An X-linked syndrome characterized by hyperuricemia, deafness, and neurological abnormalities. Lancet 1982;2:68–70.

    PubMed  Google Scholar 

  17. Becker MA, Puig JG, Mateos FA, Jiménez ML, Kim M, Simmonds A. Inherited superactivity of phosphoribosylpyrophosphate synthetase: association of uric acid over-production and sensorineural deafness. Am J Med 1988;85:383–90.

    PubMed  Google Scholar 

  18. Christen H-J, Hanefeld F, Duley JA, Simmonds HA. Distinct neurological syndrome in two brothers with hyperuricaemia. Lancet 1992;340:1167–8.

    Google Scholar 

  19. Becker MA, Losman MJ, Wilson J, Simmonds HA. Superactivity of human phosphoribosylpyrophosphate synthetase due to altered regulation by nucleotide inhibitors and inorganic phosphate. Biochim Biophys Acta 1986;882:168–76.

    PubMed  Google Scholar 

  20. Becker MA, Mejer LJ, Seegmiller JE. Gout with purine over-production due to increased phosphoribosylpyrophosphate synthetase activity. Am J Med 1973;55:232–42.

    PubMed  Google Scholar 

  21. Becker MA. Patterns of phosphoribosylpyrophosphate and ribose-5-phosphate concentration and generation in fibroblasts from patients with gout and purine overproduction. J Clin Invest 1976;57:308–18.

    PubMed  Google Scholar 

  22. Akaoka I, Fujimori S, Kamatani N, Takeuchi F, Yano E, Nishida Y, et al. A gouty family with increased phosphoribosylpyrophosphate synthetase activity: case reports, familial studies, and kinetic studies of the abnormal enzyme. J Rheumatol 1981;8:563–74.

    PubMed  Google Scholar 

  23. Becker MA, Losman MJ, Itkin P, Simkin PA. Gout with superactive phosphoribosylpyrophosphate synthetase due to increased enzyme catalytic rate. J Lab Clin Med 1982;99:485–511.

    Google Scholar 

  24. Wood AW, Becker MA, Seegmiller JE. Purine nucleotide synthesis in lymphoblasts cultured from normal subjects and a patient with Lesch-Nyhan syndrome. Biochem Genet 1973;9:261–74.

    PubMed  Google Scholar 

  25. Losman MJ, Hecker S, Woo S, Becker MA. Diagnostic evaluation of phosphoribosylpyrophosphate synthetase activities in hemolysates. J Lab Clin Med 1984;103:932–43.

    PubMed  Google Scholar 

  26. Becker MA, Losman MJ, Riman D, Kim M. PRPP synthetase superactivity in lymphoblast lines. Adv Exp Med Biol 1986;195A:51–8.

    Google Scholar 

  27. Zoref-Shani E, Sperling O. Alterations in purine metabolism in cultured fibroblasts with HGPRT deficiency and with PRPP synthetase superactivity. Adv Exp Med Biol 1980;122B:19–24.

    Google Scholar 

  28. Becker MA, Kostel PJ, Meyer LJ, Seegmiller JE. Human phosphoribosylpyrophosphate synthetase: increased enzyme specific activity in a family with gout and excessive purine synthesis. Proc Natl Acad Sci USA 1973;70:2749–52.

    PubMed  Google Scholar 

  29. Becker MA, Losman MJ, Kim M. Mechanisms of accelerated purine nucleotide synthesis in human fibroblasts with superactive phosphoribosylpyrophosphate synthetases. J Biol Chem 1987;262:5596–602.

    PubMed  Google Scholar 

  30. Zoref-Shani E, de Vries A, Sperling O. Mutant feedback resistant phosphoribosylpyrophosphate synthetase associated with purine overproduction and gout. J Clin Invest 1975;56:1093–9.

    PubMed  Google Scholar 

  31. Mateos F, García Puig J, López Jiménez M. Sobreactividad de fosforribosilpirofosfato sintetasa (PRPPs) [Phosphoribosylpyrphosphate synthetase (PRPPs) overactivity]. In: Pinto B, editor. Lithiasis renal [Renal lithiasis]. Barcelona: Ediciones Científicas y Técnicas, S.A., 1993:231–40.

    Google Scholar 

  32. Roessler BJ, Golovoy N, Palella TD, Heidler S, Becker MA. Identification of distinct PRS1 mutations in two patients with X-linked phosphoribosylpyrophosphate synthetase superactivity. Adv Exp Med Biol 1991;309B:125–30.

    PubMed  Google Scholar 

  33. Valentine WN, Paglia DE, Tartaglia AP, Gilsanz F. Hereditary hemolytic anemia with increased red cell adenosine deaminase (45-70-fold) and decreased adenosine triphosphate. Science 1977;195:783–5.

    PubMed  Google Scholar 

  34. Lesch M, Nyhan WL. A familial disorder of uric acid metabolism and central nervous system function. Am J Med 1964;36:561–70.

    PubMed  Google Scholar 

  35. Kelley WN, Greene ML, Rosenbloom FM, Henderson JF, Seegmiller JE. Hypoxanthine-guanine phosphoribosyltransferase deficiency in gout. Ann Intern Med 1969;70:155–206.

    PubMed  Google Scholar 

  36. Seegmiller JE. Contributions of Lesch-Nyhan syndrome to the understanding of purine metabolism. J Inherit Metab Dis 1989;12:184–96.

    PubMed  Google Scholar 

  37. Sculley DG, Dawson PA, Emmerson BT, Gordon RB. A review of the molecular basis of hypoxanthine-guanine phosphoribosyltransferase (HPRT) deficiency. Hum Genet 1992;90:195–207.

    PubMed  Google Scholar 

  38. Emmerson BT, Thompson L. The spectrum of hypoxanthine-guanine phosphoribosyltransferase deficiency. Q J Med 1973;42:423–40.

    PubMed  Google Scholar 

  39. de Bruyn CHMM. Hypoxanthine-guanine phosphoribosyl transferase deficiency. Hum Genet 1976;31:127–50.

    PubMed  Google Scholar 

  40. Stout JT, Caskey CT. Hypoxanthine phosphoribosyltransferase deficiency: the Lesch-Nyhan syndrome and gouty arthritis. In: Scriver CR, Beaudet AL, Sly WS, Valle D, editors. The metabolic basis of inherited disease. 6th ed. New York: McGraw-Hill, 1989:1007–28.

    Google Scholar 

  41. Cameron JS, Moro F, Simmonds HA. Gout, uric acid and purine metabolism in paediatric nephrology. Pediatr Nephrol 1993;7:105–18.

    PubMed  Google Scholar 

  42. Mizuno T. Long-term follow-up of ten patients with Lesch-Nyhan syndrome. Neuropediatrics 1986;17:158–61.

    PubMed  Google Scholar 

  43. Puig JG, Mateos FA, Jiménez ML, Arcas J, Miranda MaE, Ortíz-Vázquez JJ. Espectro clínico de la deficiencia de hipoxantina-guanina fosforribosiltransferasa: estudio de 12 pacientes [Clinical spectrum of hypoxanthine-guanine phosphoribosyltransferase: study of 12 patients]. Med Clin. In press.

  44. Catel W, Schmidt J. Über familiäre gichtische Diathese in Verdendung mit zerebralen und renalen Symptomen bei einem Kleinkind [On the diathesis of familiar gout related to the renal and cerebral symptoms of a child]. Dtsch Med Wochenschr 1959;84:2145–7.

    PubMed  Google Scholar 

  45. Watts RWE, Spellacy E, Gibbs DA, Allsop J, McKeran RO, Slavin GE. Clinical, post-mortem, biochemical and therapeutic observations on the Lesch-Nyhan syndrome with particular reference to the neurological manifestations. Q J Med 1982;51:43–78.

    PubMed  Google Scholar 

  46. Goldstein M, Anderson LT, Reuben R, Dancis J. Self-mutilation in Lesch-Nyhan disease is caused by dopaminergic denervation [letter]. Lancet 1985;1:338–9.

    Google Scholar 

  47. Anders TF, Cann HM, Ciaranello RD, Barchas JD, Berger PA. Further observations on the use of 5-hydroxytryptophan in a child with Lesch-Nyhan syndrome. Neuropediatrics 1978;9:157–66.

    Google Scholar 

  48. Rassin DK, Lloyd KG, Kelley WN, Fox IH. Decreased amino acids in various brain areas of patients with Lesch-Nyhan syndrome. N Engl J Med 1982;13:130–4.

    Google Scholar 

  49. Sidi Y, Mitchell BS. Z-nucleotide accumulation in erythrocytes from Lesch-Nyhan patients. J Clin Invest 1985;76:2416–9.

    PubMed  Google Scholar 

  50. Lloyd KG, Hornykiewicz O, Davidson L, Shannak K, Farley I, Goldstein M, et al. Biochemical evidence of dysfunction of brain neurotransmitters in the Lesch-Nyhan syndrome. N Engl J Med 1981;305:1106–11.

    PubMed  Google Scholar 

  51. Hatanaka T, Higashino H, Woo M, Yasuhara A, Sugimoto T, Kobayashi Y. Lesch-Nyhan syndrome with delayed onset of self-mutilation: hyperactivity of interneurons at the brainstem and blink reflex. Acta Neurol Scand 1990;81:184–7.

    PubMed  Google Scholar 

  52. Rijksen G, Staal GEJ, Van der Vlist MJM. Partial hypoxanthine-guanine phosphoribosyltransferase deficiency with full expression of the Lesch-Nyhan syndrome. Hum Genet 1981;57:39–47.

    PubMed  Google Scholar 

  53. Scherzer AL, Ilson JB. Normal intelligence in the Lesch-Nyhan syndrome. Pediatrics 1969;44:116–20.

    PubMed  Google Scholar 

  54. Page T, Bakay B, Nisinen E, Nyhan WL. Hypoxanthine-guanine phosphoribosyltranseferase variants: correlation of clinical phenotype with enzyme activity. J Inherit Metab Dis 1981;4:203–6.

    PubMed  Google Scholar 

  55. Nuki G, Lever J, Seegmiller JE. Biochemical characteristics of 8-azaguanine resistant human lymphoblast mutants selectedin vitro. Adv Exp Med Biol 1974;41A:255–67.

    Google Scholar 

  56. Palella TD, Silverman LJ, Schoroll CT, Homa FL, Levine M, Kelley WN. Herpes simplex virus-mediated human hypoxanthine-guanine phosphoribosyltransferase gene transfer into neuronal cells. Mol Cell Biol 1988;8:457–60.

    PubMed  Google Scholar 

  57. Zoref-Shani E, Sperling O. Dependence of the metabolic fate of IMP on the rate of total IMP synthesis. Studies in cultured fibroblasts from normal subjects and from purine-overproducing mutant patients. Biochim Biophys Acta 1980;607:503–11.

    PubMed  Google Scholar 

  58. Vincent MF, Van den Berghe G, Hers HG. Effect of fructose on the concentration of phosphoribosyltransferase in isolated hepatocytes. Adv Exp Med Biol 1986;195B:615–21.

    Google Scholar 

  59. Brenton DP, Astria K, Cruikshank MK, Seegmiller JE. Measurement of free nucleotides in cultured human lymphoid cells using high pressure liquid chromatography. Biochem Med 1977;17:271–4.

    Google Scholar 

  60. Lommen EJP, Vogels GD, Van der Zee SPM, Trijbels JMF, Schretlen EDAM. Concentrations of purine nucleotides in erythrocytes of patients with the Lesch-Nyhan syndrome before and during oral administration of adenine. Acta Pediatr Scand 1971;60:642–6.

    Google Scholar 

  61. Rivard GE, Izadi P, Lazerson J, McLaren JD, Parker C, Fish CH. Functional and metabolic studies of platelets from patients with Lesch-Nyhan syndrome. Br J Haematol 1975;31:245–53.

    PubMed  Google Scholar 

  62. Greene ML, Boyle JA, Seegmiller JE. Substrate stabilization: genetically controlled reciprocal relationship of two human enzymes. Science 1970;167:887–9.

    PubMed  Google Scholar 

  63. Watts RWE, Watts JEM, Seegmiller JE. Xanthine oxidase activity in human tissues and its inhibition by allopurinol. J Lab Clin Med 1965;66:688–97.

    PubMed  Google Scholar 

  64. Jarasch E-D, Grund C, Bruder G, Heid HW, Keenan TW, Franke WW. Localization of xanthine oxidase in mammary-gland epithelium and capillary endothelium. Cell 1981;25:67–82.

    PubMed  Google Scholar 

  65. Puig JG, Mateos FA, Jiménez ML, Conthe PG. Renal handling of uric acid in gout: impaired tubular transport of urate not dependent on serum urate levels. Metabolism 1986;35:1147–53.

    PubMed  Google Scholar 

  66. Yü T-F, Balis EA, Krenitsky TA, Dancis J, Silvers DN, Elion GB, et al. Rarity of X-linked partial hypoxanthine-guanine phosphoribosyltransferase deficiency in a large gouty population. Ann Intern Med 1972;76:255–64.

    PubMed  Google Scholar 

  67. Van den Berghe G, Hers HG. Abnormal AMP deaminase in primary gout [letter]. Lancet 1980;2:1090.

    Google Scholar 

  68. Seegmiller JE, Klinenberg JR, Miller J, Watts RWE. Suppression of glycine-15N incorporation into urinary uric acid by adenine-8-13C in normal and gouty subjects. J Clin Invest 1968;47:1193–203.

    PubMed  Google Scholar 

  69. Fox IH. Adenosine triphosphate degradation in specific disease. J Lab Clin Med 1985;106:101–10.

    PubMed  Google Scholar 

  70. Fox IH, Kelley WN. Studies on the mechanism of fructose-induced hyperuricemia. Metabolism 1972;21:713–21.

    PubMed  Google Scholar 

  71. Puig JG, Jiménez ML, Mateos FA, Fox IH. Adenine nucleotide turnover in hypoxanthine-guanine phosphoribosyl-transferase deficiency: evidence for an increased contribution of purine biosynthesisde novo. Metabolism 1989;38:410–8.

    PubMed  Google Scholar 

  72. Bode JC, Zelder O, Rumpelt HJ, Wittkamp U. Depletion of liver adenosine phosphates and metabolic effects of intravenous infusion of fructose or sorbitol in man and in the rat. Eur J Clin Invest 1973;3:436–41.

    PubMed  Google Scholar 

  73. Fox IH. Metabolic basis for disorders of purine nucleotide degradation. Metabolism 1981;30:616–34.

    PubMed  Google Scholar 

  74. Mock DM, Perman JA, Thaler MM, Morris RC Jr. Chronic fructose intoxication after infancy in children with hereditary fructose intolerance: a cause of growth retardation. N Engl J Med 1983;309:764–70.

    PubMed  Google Scholar 

  75. Oberhaensli RD, Rajagopalan B, Taylor DJ, Radda GK, Collins JE, Leonard JV, et al. Study of hereditary fructose intolerance by use of31P magnetic resonance spectroscopy. Lancet 1987;2:931–4.

    PubMed  Google Scholar 

  76. Dieppe PA. Investigation and management of gout in the young and the elderly. Ann Rheum Dis 1989;91:263–6.

    Google Scholar 

  77. Sutton JR, Toews CJ, Ward GR, Fox IH. Purine metabolism during strenuous muscular exercise in man. Metabolism 1980;29:254–60.

    PubMed  Google Scholar 

  78. Ketai LH, Simon RH, Kreit JW, Grum CM. Plasma hypoxanthine and exercise. Am Rev Respir Dis 1987;136:98–101.

    PubMed  Google Scholar 

  79. Mineo I, Kono N, Hara N, Shimizu T, Yamada Y, Kawachi M, et al. Myogenic hyperuricemia. A common pathophysiologic feature of glycogenosis types III, V, and VII. N Engl J Med 1987;317:75–80.

    PubMed  Google Scholar 

  80. Puig JG, de Miguel E, Mateos FA, Miranda MaE, Romera NM, Espinosa A. McArdle's disease and gout. Muscle Nerve 1992;15:822–8.

    PubMed  Google Scholar 

  81. Mineo I, Kono N, Shimizu T, Hara N, Yamada Y, Sumi S, et al. Excess purine degradation in exercising muscles of patients with glycogen storage disease types V and VII. J Clin Invest 1985;76:556–60.

    PubMed  Google Scholar 

  82. Hers H-G, Van Hoof F, de Barsy T. Glycogen storage diseases. In: Scriver CR, Beaudet AL, Sly WS, Valle D, editors. The metabolic basis of inherited disease. 6th ed. New York: McGraw-Hill, 1989:425–52.

    Google Scholar 

  83. Alepa FP, Howell RR, Klinenberg JR, Seegmiller JE. Relationships between glycogen storage disease and tophaceous gout. Am J Med 1967;42:58–66.

    PubMed  Google Scholar 

  84. Roe TF, Kogut MD. The pathogenesis of hyperuricemia in glycogen storage disease, type I. Pediatr Res 1977;11:664–9.

    PubMed  Google Scholar 

  85. Cohen JL, Vinik A, Faller J, Fox IH. Hyperuricemia in glycogen storage disease type I: contributions by hypoglycemia and hyperglucagonemia to increased urate production. J Clin Invest 1985;75:251–7.

    PubMed  Google Scholar 

  86. Faller J, Fox IH. Ethanol-induced hyperuricemia: evidence for increased urate production by activation of adenine nucleotide turnover. N Engl J Med 1982;307:1598–602.

    PubMed  Google Scholar 

  87. Puig JG, Fox IH. Ethanol-induced activation of adenine nucleotide turnover: evidence for a role of acetate. J Clin Invest 1984;74:936–41.

    PubMed  Google Scholar 

  88. Tekkanat KK, Port FK, Schmaltz S, Chen T, Fox IH. Excessive ATP degradation during hemodialysis against sodium acetate. J Lab Clin Med 1988;112:686–93.

    PubMed  Google Scholar 

  89. O'Connor LR, Wheeler WS, Bethune JE. Effect of hypophosphatemia on myocardial performance in man. N Engl J Med 1977;297:901–3.

    PubMed  Google Scholar 

  90. Knochel JP, Barcenas C, Cotton JR, Fuller TJ, Haller R, Carter NW. Hypophosphatemia and rhabdomyolysis. J Clin Invest 1978;62:1240–6.

    PubMed  Google Scholar 

  91. Grum CM, Simon RH, Dantzker DR, Fox IH. Evidence for ATP degradation in critically ill patients. Chest 1985;88:763–7.

    PubMed  Google Scholar 

  92. Wooliscroft JO, Fox IH. Increased body fluid purine levels during hypotensive events. Am J Med 1986;81:472–8.

    PubMed  Google Scholar 

  93. Hasday JD, Grum CM. Nocturnal increase of urinary uric acid:creatinine ratio. A biochemical correlate of sleep associated hypoxemia. Am Rev Respir Dis 1987;135:534–8.

    PubMed  Google Scholar 

  94. Wooliscroft JO, Colfer H, Fox IH. Hyperuricemia in acute illness: a poor prognostic sign. Am J Med 1982;72:59–62.

    Google Scholar 

  95. Saugstad OD. Hypoxanthine as an indicator of hypoxia: its role in health and disease through free radical production. Pediatr Res 1988;23:143–50.

    PubMed  Google Scholar 

  96. Mateos FA, Puig JG, Ramos TH, Carranza RH, Miranda ME, Gasalla RC. Erythrocyte ATP (iATP) as an indicator of neonatal hypoxia. Adv Exp Med Biol 1989;253A:345–52.

    PubMed  Google Scholar 

  97. Mateos FA, Gómez PF, Puig JG, Jiménez ML, Ramos TH, Mantilla JG. Enhanced adenine nucleotide degradation in chronic obstructive pulmonary disease: the effect of oxygen therapy. Adv Exp Med Biol 1991;253A:333–8.

    Google Scholar 

  98. Mateos FA, Díaz V, Puig JG, Ramos TH, Jiménez ML, Díaz E, et al. Adenine nucleotide metabolism in liver ischemia: effect of allopurinol. Adv Exp Med Biol 1991;309A:301–4.

    PubMed  Google Scholar 

  99. Edwards NL, Recker D, Airozo D, Fox IH. Enhanced purine salvage during allopurinol therapy: an important pharmacologic property in humans. J Lab Clin Med 1981;98:673–83.

    PubMed  Google Scholar 

  100. Mateos FA, Puig JG, Jiménez ML, Fox IH. Hereditary xanthinuria: evidence for enhanced hypoxanthine salvage. J Clin Invest 1987;79:847–52.

    PubMed  Google Scholar 

  101. Gold MS, Williams JC, Spivack M, Grann V. Sickle cell anemia and hyperuricemia. JAMA 1968;206:1572–3.

    PubMed  Google Scholar 

  102. Paik CH, Alavi I, Dunea G, Weiner L. Thalassaemia and gouty arthritis. JAMA 1970;213:296–7.

    PubMed  Google Scholar 

  103. Liberman UA, Samuel R, Halabe A, Joshua H, Lubin E, Zoref-Shani E, et al. Juvenile metabolic gout caused by chronic compensated hemolytic syndrome. Arthritis Rheum 1982;25:1264–6.

    PubMed  Google Scholar 

  104. Talbott JH. Gout and blood dyscrasias. Medicine (Baltimore) 1959;38:173–205.

    Google Scholar 

  105. Simmonds HA, Cameron JS, Morris GS, Davies PM. Allopurinol in renal failure and the tumor lysis syndrome. Clin Chim Acta 1986;160:189–95.

    PubMed  Google Scholar 

  106. Eisen AZ, Seegmiller JE. Uric acid metabolism in psoriasis. J Clin Invest 1961;40:1486–94.

    PubMed  Google Scholar 

  107. Puig JG, Mateos FA, Jiménez ML, Gómez PL, Michán AA, Vázquez JO. Uric acid metabolism in psoriasis. Adv Exp Med Biol 1986;195A:411–6.

    Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Division of Internal Medicine, ‘La Paz’ Hospital, Universidad Autónoma, Madrid, Spain

    J. García Puig

  2. Division of Clinical Biochemistry, ‘La Paz’ Hospital, Universidad Autónoma, Madrid, Spain

    F. Antón Mateos

Authors
  1. J. García Puig
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. F. Antón Mateos
    View author publications

    You can also search for this author in PubMed Google Scholar

Rights and permissions

Reprints and permissions

About this article

Cite this article

Puig, J.G., Mateos, F.A. Clinical and biochemical aspects of uric acid overproduction. Pharm World Sci 16, 40–54 (1994). https://doi.org/10.1007/BF01880655

Download citation

  • Accepted:

  • Issue Date:

  • DOI: https://doi.org/10.1007/BF01880655

Keywords

Search

Navigation