Advertisement

Current Rheumatology Reports

, Volume 8, Issue 3, pp 215–223 | Cite as

New developments in the epidemiology and genetics of gout

  • Raihana Zaka
  • Charlene J. WilliamsEmail author
Article

Abstract

The prevalence of gout appears to be rapidly increasing worldwide and is no longer a disorder suffered primarily by over-fed alcohol consumers. Emerging risk factors include longevity, metabolic syndrome, and new classes of pharmacologic agents. In some ethnic populations, no obvious risk factors can explain the high incidence of hyperuricemia and gout, suggesting a genetic liability. Studies to identify genes associated with gout have included families with defects in purine metabolism, as well as families in whom the occurrence of gout is secondary to renal disorders such as juvenile hyperuricemic nephropathy and medullary cystic kidney disease. Case-control studies of isolated aboriginal cohorts suffering from primary gout have revealed several chromosomal loci that may harbor genes that are important to the development and/or progression of gout.

Keywords

Uric Acid Gout Hyperuricemia Serum Uric Acid Level Gouty Arthritis 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References and Recommended Reading

  1. 1.
    Luk AJ, Simkin PA: Epidemiology of hyperuricemia and gout. Am J Manag Care 2005, 11:S435-S442.Excellent new review of the epidemiology of gout, especially with respect to the relationship between metabolic syndrome and goutPubMedGoogle Scholar
  2. 2.
    Healey LA: The epidemiology of Filipino hyperuricemia. In Gout, Hyperuricemia and Other Crystal-associated Arthropathies. Edited by Smyth CJ, Holers VM. New York: Marcel Dekker; 1999:121–126.Google Scholar
  3. 3.
    Baker JF, Krishnan E, Chen I, Schumacher HR: Serum uric acid and cardiovascular disease: recent developments and where do they leave us? Am J Med 2005, 118:816–826.PubMedCrossRefGoogle Scholar
  4. 4.
    Johnson RJ, Kang DH, Feig D, et al.: Is there a pathogenetic role for uric acid in hypertension and cardiovascular and renal disease? Hypertension 2003, 41:1183–1190.PubMedCrossRefGoogle Scholar
  5. 5.
    Gerns GAA, Lanham J, Dieppe P, Galston DJ: DNA polymorphism of an apoprotein gene associates with the hypertriglyceridemia of primary gout. Hum Genet 1988, 78:55–59.CrossRefGoogle Scholar
  6. 6.
    Moriwaki Y, Yamamoto T, Takahashi S, et al.: Apoprotein E phenotype in patients with gout: relation with hypertriglygeridemia. Ann Rheum Dis 1995, 54:351–354.PubMedCrossRefGoogle Scholar
  7. 7.
    Tipene-Leach D, Pahau H, Joseph N, et al.: Insulin resistance in a rural Maori community. N Z Med J 2004, 117:U1208.PubMedGoogle Scholar
  8. 8.
    Gonzalez EB, Miller SB, Agudelo CA: Optimal management of gout in older patients. Drugs Aging 1994, 4:128–134.PubMedCrossRefGoogle Scholar
  9. 9.
    Clive DM: Renal transplant-associated hyperuricemia and gout. J Am Soc Nephrol 2000, 11:974–979.PubMedGoogle Scholar
  10. 10.
    Lin HY, Rocher LI, McQuillan MA, et al.: Cyclosporine induced hyperuricemia and gout. N Engl J Med 1989, 321:287–292.PubMedCrossRefGoogle Scholar
  11. 11.
    Burack DA, Griffith BP, Thompson ME, Kahl LE: Hyperuricemia and gout among transplant recipients receiving cyclosporine. Am J Med 1992, 92:141–146.PubMedCrossRefGoogle Scholar
  12. 12.
    Wallace KL, Riedel AA, Joseph-Ridge N, Wortmann R: Increasing prevalence of gout and hyperuricemia over 10 years among older adults in a managed care population. J Rheumatol 2004, 31:1582–1587.This recent epidemiology study describes the increase in gout prevalence in the United States, and association with gender and agePubMedGoogle Scholar
  13. 13.
    Arromdee E, Michet CJ, Crowson CS, et al.: Epidemiology of gout: is the incidence rising? J Rheumatol 2002, 29:2403–2406.This recent epidemiology study shows the increase in prevalence of gout using a cohort from the Rochester Epidemiology Project.PubMedGoogle Scholar
  14. 14.
    Harris CM, Lloyd DC, Lewis J: The prevalence and prophylaxis of gout in England. J Clin Epidemiol 1995, 48:1153–1158.PubMedCrossRefGoogle Scholar
  15. 15.
    Mikuls TR, Farrar JT, Bilker WB, et al.: Gout epidemiology: results from the UK General Practice Research Database. Ann Rheum Dis 2005, 64:267–272.This study is the most recent description of gout in the UK population where the steep increase in the rise in gout incidence has slowedPubMedCrossRefGoogle Scholar
  16. 16.
    Zeng Q, Wang Q, Chen R, et al.: Primary gout in Shantou: a clinical and epidemiological study. Chin Med J (Engl) 2003, 116:66–69.Google Scholar
  17. 17.
    Chang HY, Pan WH, Yeh WT, Tsai KS: Hyperuricemia and gout in Taiwan: results from the Nutritional and Health Survey in Taiwan (1993-1996). J Rheumatol 2001, 28:1640–1646.PubMedGoogle Scholar
  18. 18.
    Yu KH, Luo SF: Younger age at onset of gout in Taiwan. Rheumatol (Oxford) 2003, 42:166–170.CrossRefGoogle Scholar
  19. 19.
    Chen S-Y, Chen C-L, Shen M-L, Kamatani N: Trends in the manifestations of gout in Taiwan. Rheumatol 2003, 42:1529–1533.CrossRefGoogle Scholar
  20. 20.
    Klemp P, Stansfield SA, Castle B, Robertson MC: Gout is on the increase in New Zealand. Ann Rheum Dis 1997, 56:22–26.PubMedCrossRefGoogle Scholar
  21. 21.
    Choi HK, Liu S, Curhan G: Intake of purine-rich foods, protein, dairy products and serum uric acid levels: the Third National Health and Nutrition Examination Survey. Arthritis Rheum 2005, 52:283–2890.This new study explores the relationship, from an epidemiologic perspective, between gout incidence and ingestion of a purinerich dietPubMedCrossRefGoogle Scholar
  22. 22.
    Choi HK, Atkinson K, Karlson EW, et al.: Alcohol intake and risk of incident gout in men: a prospective study. Lancet 2004, 363:1277–1281.PubMedCrossRefGoogle Scholar
  23. 23.
    Choi HK, Curhan G: Gout: epidemiology and lifestyle choices. Curr Opin Rheum 2005, 17:341–345.Good review of recent epidemiology studies of gout/hyperuricemia and association with risk factors such as diet, hypertension, and so on.CrossRefGoogle Scholar
  24. 24.
    Bellowood P: The Autronesian dispersal and the origin of languages. Sci Am 1991, 256:70–75.Google Scholar
  25. 25.
    Chou CT, Lai JS: The epidemiology of hyperuricemia and gout in Taiwan Aborigines. Br J Rheum 1998, 37:258–262.CrossRefGoogle Scholar
  26. 26.
    Roberts-Thomson RA, Roberts-Thomson PJ: Rheumatic disease and the Australian Aborigine. Ann Rheum Dis 1999, 58:266–270.PubMedCrossRefGoogle Scholar
  27. 27.
    Chin G, Segasothy M: Gouty arthritis in Australian aborigines. Aust NZ J Med 2000, 30:639–640.Google Scholar
  28. 28.
    Emmerson BT, Douglas W, Doherty RL, Feigl P: Serum urate concentrations in the Australian Aboriginal. Ann Rheum Dis 1969, 28:150–155.PubMedCrossRefGoogle Scholar
  29. 29.
    Chan KH, Segasothy M: Gouty arthritis in Australian Aboriginals: more common than previously suspected. Med J Aus 2004, 181:172.Google Scholar
  30. 30.
    Brauer GW, Prior IAM: A prospective study of gout in New Zealand Maoris. Ann Rheum Dis 1978, 37:466–472.PubMedCrossRefGoogle Scholar
  31. 31.
    Gibson T, Waterworth R, Hatfield P, et al.: Hyperuricemia, gout, and kidney finction in New Zealand Maori men. Br J Rheumatol 1984, 23:276–282.PubMedCrossRefGoogle Scholar
  32. 32.
    Prior IAM: Epidemiology of rheumatic disorders in the Pacific with particular emphasis on hyperuricemia and gout. Semin Arthritis Rheum 1981, 11:213–219.PubMedCrossRefGoogle Scholar
  33. 33.
    Simmonds HA, McBride MB, Hatfield PJ, et al.: Polynesian women are also at risk for hyperuricemia and gout because of a genetic defect in renal tubule handling. Br J Rheumatol 1994, 33:932–937.PubMedCrossRefGoogle Scholar
  34. 34.
    Hauge M, Harvald B: Heredity in gout and hyperuricemia. Acta Med Scand 1955, 152:247–257.PubMedCrossRefGoogle Scholar
  35. 35.
    Auscher C, Pasquier C, de Gery A, et al.: Xanthinuria: study of a large kindred with familial urolithiasis and gout. Biomedicine 1977, 27:57–59.PubMedGoogle Scholar
  36. 36.
    Kelley W, Rosenbloom F, Henderson F, Seegmiller E: A specific enzyme defect in gout associated with overproduction of uric acid. Proc Natl Acad Sci U S A 1967, 57:1735–1739.PubMedCrossRefGoogle Scholar
  37. 37.
    Sperling O, Boer P, Persky-Brosh S, et al.: Altered kinetic property of erythrocyte phosphoribosylpyrophosphate synthetase in excessive purine production. Eur J Clin Biol Res 1972, 17:703–706.Google Scholar
  38. 38.
    Becker M, Kostel P, Meyer L, Seegmiller E: Human phosphorybosilpyrophosphatase synthetase: increased enzyme specific activity in a family with gout and excessive purine synthesis. Proc Nat Acad Sci U S A 1973, 70:2749–2752.CrossRefGoogle Scholar
  39. 39.
    Becker MA, Meyer LJ, Wood AW, Seegmiller JE: Purine overproduction in man associated with increased phosphoribosylpyrophosphate synthetase activity. Science 1973, 179:1123–1126.PubMedCrossRefGoogle Scholar
  40. 40.
    Akaoka I, Fujimori S, Kamatani N, et al.: A gouty family with increased phosphoribosylpyrophosphate synthetase activity: case reports, familial studies, and kinetic studies of the abnormal enzyme. J Rheumatol 1981, 8:563–574.PubMedGoogle Scholar
  41. 41.
    Roessler B, Palella T, Heidler S, Becker M: Identification of distinct PRPS1 mutations in two patients with X-linked phosphoribosylpyrophosphate synthetase superativity [abstract]. Clin Res 1991, 39:267A.Google Scholar
  42. 42.
    Christen H-J, Hanefeld F, Duley JA, Simmonds HA: Distinct neurological syndrome ine to brothers with hyperuricemia. Lancet 1992, 340:1167–1168.PubMedCrossRefGoogle Scholar
  43. 43.
    Becker M, Smith P, Taylor W, et al.: The genetic and functional basis of purine nucleotide feedback-resistant phosphoribosylpyrophosphate synthetase superactivity. J Clin Invest 1995, 96:2133–2141.PubMedCrossRefGoogle Scholar
  44. 44.
    Becker M, Taylor W, Smith P, Ahmed M: Overexpression of the normal phosphoribosylpyrophosphate synthetase 1 isoform underlies catalytic superactivity of human phosphoribosylpyrophosphate synthetase. J Biol Chem 1996, 271:19894–19899.PubMedCrossRefGoogle Scholar
  45. 45.
    Thompson G, Weiss J, Goldman R, Rigg G: Familial occurrence of hyperuricemia, gout, and medullary cystic disease. 1978, 138:1614-1617.Google Scholar
  46. 46.
    Simmonds HA, Warren DJ, Cameron JS, et al.: Familial gout and renal failure in young women. Clin Nephrol 1980, 14:176–182.PubMedGoogle Scholar
  47. 47.
    Warren D, Simmonds H, Gibson T, Naik R: Familial gout and renal failure. Arch Dis Child 1981, 56:699–704.PubMedCrossRefGoogle Scholar
  48. 48.
    Leumann EP, Wegmann W: Familial nephropathy with hyperuricemia and gout. Nephron 1983, 34:51–57.PubMedCrossRefGoogle Scholar
  49. 49.
    MacDermot K, Allsop J, Watts R: The rate of purine synthesis de nova in blood mononuclear cells in vitro from patients with familial hyperuricaemic nephropathy. Clin Sci (Lond) 1984, 67:249–258.Google Scholar
  50. 50.
    Yokota N, Yamanaka H, Yamamoto Y, et al.: Autosomal dominant transmission of gouty arthritis with renal disease in a large Japanese family. Ann Rheum Dis 1991, 50:108–111.PubMedCrossRefGoogle Scholar
  51. 51.
    Duncan H, Dixon ACJ: Gout, familial hyperuricemia and renal disease. Q J Med 1960, 29:127–136.PubMedGoogle Scholar
  52. 52.
    McBride MB, Simmonds HA, Moro F: Genetic gout in childhood:familial juvenile hyperuricemic nephropathy or "familial renal disease". J Inher Metab Dis 1997, 20:351–353.PubMedCrossRefGoogle Scholar
  53. 53.
    Rosenbloom FM, Kelley WN, Carr AA, Seegmiller JE: Familial nephropathy and gout in a kindred. Clin Res 1967, 15:270.Google Scholar
  54. 54.
    Van Goor W, Kooiker CJ, Mees FJD: An unusual form of renal disease associated with gout and hypertension. J Clin Path 1971, 24:354–359.PubMedCrossRefGoogle Scholar
  55. 55.
    Massari PU, Hsu CH, Barnes RV, et al.: Familial hyperuricemia and renal disease. Arch Intern Med 1980, 140:680–684.PubMedCrossRefGoogle Scholar
  56. 56.
    Calabrese G, Simmonds HA, Cameron JS, Davies PM: Precocious familial gout with reduced fractional urate clearance and normal purine enzymes. Quart J Med 1990, 277:441–450.Google Scholar
  57. 57.
    Cameron JS, Ogg CS, Moro F, et al.: Precocious familial gout. Lancet 1990, 336:745.PubMedCrossRefGoogle Scholar
  58. 58.
    Moro F, Ogg CS, Simmonds HA, et al.: Familial juvenile gouty nephropathy with renal urate hyposecretion preceeding renal disease. Clin Nephrol 1991, 35:263–269.PubMedGoogle Scholar
  59. 59.
    Saeki A, Hosoya T, Okabe H, et al.: Newly discovered familial juvenile gouty nephropathy in a Japanese family. Nephron 1995, 70:359–366.PubMedCrossRefGoogle Scholar
  60. 60.
    Kamatani N, Moritani M, Yamanaka H, et al.: Localization of a gene for familial juvenile hyperuricemic nephropathy causing under-excretion type gout to 16p12 by genome-wide linkage analysis of a large family. Arthritis Rheum 2000, 43:925–929.This is the.rst report of a parametric linkage analysis in a single large family displaying familial juvenile hyperuricemic nephropathyPubMedCrossRefGoogle Scholar
  61. 61.
    Stacey JM, Turner JJO, Harding B, et al.: Genetic mapping studies of familial juvenile hyperuricemic nephropathy on chromosome 16p13-p11. J Clin Endocr Metab 2003, 88:464–470.PubMedCrossRefGoogle Scholar
  62. 62.
    Goldman SH, Walker SR, Merigan TC Jr, et al.: Hereditary occurrence of cystic disease of the renal medulla. New Eng J Med 1966, 274:984–992.PubMedCrossRefGoogle Scholar
  63. 63.
    Gardner KD Jr: Evolution of clinical signs in adult-onset cystic disease of the renal medulla. Ann Intern Med 1971, 74:47–54.PubMedGoogle Scholar
  64. 64.
    Christodoulou K, Tsingis M, Stavrou C, et al.: Chromosome localization of a gene for autosomal dominant medullary cystic kidney disease (ADMCKD). Hum Mol Genet 1998, 7:905–911.PubMedCrossRefGoogle Scholar
  65. 65.
    Fuchshuber A, Kroiss S, Karle S, et al.: Refinement of the gene locus for autosomal dominant medullary cystic kidney disease type 1 (MCKD1) and construction of a physical and partial transcriptional map of the region. Genomics 2001, 72:278–284.PubMedCrossRefGoogle Scholar
  66. 66.
    Wolf MTF, Van Vlem B, Hennies HC, et al.: Telomeric refinement of the MCKD1 locus on chromosome 1q21. Kid Int 2004, 66:580–585.This study describes the most recent refinement on the locus for autosomal dominant medullary cystic kidney disease 1.CrossRefGoogle Scholar
  67. 67.
    Scolari F, Puzzer D, Amoroso A, et al.: Identification of a new locus for medullary cystic disease on chromosome 16p12. Am J Hum Genet 1999, 64:1655–1660.PubMedCrossRefGoogle Scholar
  68. 68.
    Dahan K, Fuchshuber A, Adamis S, et al.: Familial juvenile hyperuricemic nephropathy and autosomal dominant medullary cystic kidney disease type 2. Two facets of the same disease? J Am Soc Nephrol 2001, 12:2348–2357.PubMedGoogle Scholar
  69. 69.
    Scolari F, Viola BF, Ghiggeri GM, et al.: Towards the identification of (a) gene(s) for autosomal dominant medullary cystic kidney disease. J Nephrol 2003, 16:321–328.PubMedGoogle Scholar
  70. 70.
    Hart TC, Gorry MC, Hart PS, et al.: Mutations of the UMOD gene are responsible for medullary cystic kidney disease 2 and familial juvenile hyperuricemic nephropathy. J Med Genet 2002, 39:882–892.This is the first report of UMOD mutations in patients with FJHN and MCKD.PubMedCrossRefGoogle Scholar
  71. 71.
    Malagolini N, Cavallone D, Serafini-Cessi F: Intracellular transport, cell-surface exposure and release of recombinant Tamm-Horsfall glycoprotein. Kidney Int 1997, 52:1340–1350.PubMedCrossRefGoogle Scholar
  72. 72.
    Hoyer JR, Sisson SP, Vernier RL: Tamm-Horsfall glycoprotein: ultrastructural immunoperoxidase localization in rat kidney. Lab Invest 1979, 41:168–173.PubMedGoogle Scholar
  73. 73.
    Zager RA, Coltran RS, Hoyer JR: Pathologic localization of Tamm-Horsfall protein in interstitial deposits in renal disease. Lab Invest 1978, 38:52–57.PubMedGoogle Scholar
  74. 74.
    Resnick JS, Sisson S, Vernier RL: Tamm-Horsfall protein: abnormal localization in renal disease. Lab Invest 1978, 38:550–555.PubMedGoogle Scholar
  75. 75.
    Turner JJ, Stacey JM, Harding B, et al.: Uromodulin mutations cause familial juvenile hyperuricemic nephropathy. J Clin Endocrinol Metab 2003, 88:1398–1401.The first report of mutations in the UMOD gene causing familial juvenile hyperuricemic nephropathyPubMedCrossRefGoogle Scholar
  76. 76.
    Wolf MTF, Mucha BE, Attanasio M, et al.: Mutations in the uromodulin gene in MCKD type 2 patients cluster exon 4 which codes three EGF-like domains. Kidney Int 2003, 64:1580–1587.First report of mutations in the UMOD gene as the cause of autosomal dominant medullary cystic kidney disease 2, confirming the allelism between familial juvenile hyperuricemic nephropathy and medullary cystic kidney disease 2PubMedCrossRefGoogle Scholar
  77. 77.
    Bleyer AJ, Trachtman H, Sandhu J, et al.: Renal manifestations of a mutation in the uromodulin (Tamm Horsfall protein) gene. Am J Kidney Dis 2003, 42:E20-E26.PubMedCrossRefGoogle Scholar
  78. 78.
    Kudo E, Kamatani N, Tezuka O, et al.: Familial juvenile hyperuricemic nephropathy: detection of mutations in the uromodulin gene in five Japanese families. Kidney Int 2004, 65:1589–1597.PubMedCrossRefGoogle Scholar
  79. 79.
    Rezende-Lima W, Parreira KS, Garcia-Gonzalez M, et al.: Homozygosity for uromodulin disorders: FJHN and MCKD-type 2. Kidney Int 2004, 66:558–563.This recent study describes the relative phenotypes of FJHN and ADMCKD2 individuals affected with heterozygous vs. homozygous mutations in UMODPubMedCrossRefGoogle Scholar
  80. 80.
    Bleyer AJ, Hart TC, Shihabi Z, et al.: Mutations in the uromodulin gene decrease urinary excretion of Tamm-Horsfall protein. Kidney Int 2004, 66:974–977.This study describes functional consequences of UMOD mutations.PubMedCrossRefGoogle Scholar
  81. 81.
    Kumar S: Tamm-Horsfall protein-uromodulin (1950-1990). Kidney Int 1990, 37:1395–1401.PubMedCrossRefGoogle Scholar
  82. 82.
    Huan Y, Van Adelsburg J: Polycistin-1, the PKD1 gene product, is in a complex containing E-cadherin and the catenins. J Clin Invest 1999, 104:1459–1468.PubMedCrossRefGoogle Scholar
  83. 83.
    Nurnberger J, Bacallao RL, Phillips CL: Inversin forms a complex with catenins and N-cadherin in polarized epithelial cells. Mol Biol Cell 2002, 13:3096–3106.PubMedCrossRefGoogle Scholar
  84. 84.
    Vos HL, Devarayalu S, deVries Y, Bornstein P: Thrombospondin 3, a new member of the thrombospondin gene famile. J Biol Chem 1992, 267:12192–12196.PubMedGoogle Scholar
  85. 85.
    Hugo C: The thrombospondin 1-TGF beta axis in.brotic renal disease. Nephrol Dial Transplant 2003, 18:1241–1245.PubMedCrossRefGoogle Scholar
  86. 86.
    Ohno I, Ichida K, Okabe H, et al.: Familial juvenile gouty nephropathy: exclusion of 16p12 from the candidate locus. Nephron 2002, 92:573–575.PubMedCrossRefGoogle Scholar
  87. 87.
    Ichida K, Hosoyamada M, Kimura H, et al.: Urate transport via human PAH transporter hOAT1 and its gene structure. Kidney Int 2003, 63:143–155.PubMedCrossRefGoogle Scholar
  88. 88.
    Enomoto A, Kimura H, Chairoungdua A, et al.: Molecular identification of a renal urate-anion exchanger that regulates blood urate levels. Nature 2002, 417:447–452.PubMedGoogle Scholar
  89. 89.
    Tanaka M, Itoh K, Matsushita K, et al.: Two male siblings with hereditary renal hypouricemia and exerciseinduced ARF. Am J Kidney Dis 2003, 42:1287–1292.PubMedCrossRefGoogle Scholar
  90. 90.
    Tureci O, Schmitt H, Fadle N, et al.: Molecular definition of a novel human galectin which is immunogenic in patients with Hodgkin’s disease. J Biol Chem 1997, 272:6416–6422.PubMedCrossRefGoogle Scholar
  91. 91.
    Lipkowitz MS, Leal-Ointo E, Rappoport JZ, et al.: Functional reconstruction, membrane targeting, genomic structure and chromosomal localization of a human urate transporter. J Clin Invest 2001, 107:1103–1115.PubMedCrossRefGoogle Scholar
  92. 92.
    Bingham C, Ellard S, van’t Hoff WG, et al.: Atypical familial juvenile hyperuricemic nephropathy associated with a hepatocyte nuclear factor -1b gene mutation. Kidney Int 2003, 63:1645–1651.This is the.rst description of mutations in HNF-1β in familial juvenile hyperuricemic nephropathy patients.PubMedCrossRefGoogle Scholar
  93. 93.
    Mendel DB, Hansen LP, Graves MK, et al.: HNF-1alpha and HNF-1beta (vHNF-1) share dimerization and homeodomains, but not activation domains, and form heterodimers in vitro. Genes Dev 1991, 5:1042–1056.PubMedCrossRefGoogle Scholar
  94. 94.
    Lazzaro D, de Simone V, de Magistris L, et al.: LFB1 and LFB3 homeoproteins are sequentially expressed during kidney development. Development 1992, 114:469–479.PubMedGoogle Scholar
  95. 95.
    Hodanova K, Majewski J, Kublova M, et al.: Mapping of a new candidate locus for uromodulin-associated kidney disease (UAKD) to chromosome 1q41. Kid Int 2005, 68:1472–1482.This new study details the genetic analyses of several hyperuricemic nephropathy families whose defect has not been genetically mapped and it identifies a new locus for this class of disorders on chromosome 1q41CrossRefGoogle Scholar
  96. 96.
    Cheng LS-C, Chiang S-L, Tu H-P, et al.: Genome-wide scan for gout in Taiwanese aborigines reveals linkage to chromosome 4q25. Am J Hum Genet 2004, 75:498–503.This is the first description of a significant genetic linkage to a chromosomal locus in an isolated population with a high prevalence of primary gout.PubMedCrossRefGoogle Scholar
  97. 97.
    Wang WH, Chang SJ, Wang TN, et al.: Complex segregation and linkage analysis of familial gout in Taiwanese aborigines. Arthritis Rheum 2004, 50:242–246.This recent study identified an additional locus for hyperuricemia and gout in the Taiwanese Aboriginal populationPubMedCrossRefGoogle Scholar
  98. 98.
    Puca AA, Daly MJ, Brewster SJ, et al.: A genome wide scan for linkage to human exceptional longevity identifies a locus on chromosome 4. Proc Natl Acad Sci U S A 2001, 98:10505–10508.PubMedCrossRefGoogle Scholar
  99. 99.
    Cutler RG: Urate and ascorbate: their possible roles as antioxidants in determining longevity of mammalian species. Arch Gerontol Geriatr 1984, 3:321–348.PubMedCrossRefGoogle Scholar

Copyright information

© Current Science Inc 2006

Authors and Affiliations

  1. 1.Department of Medicine, Division of RheumatologyThomas Jefferson UniversityPhiladelphiaUSA

Personalised recommendations