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Rheum Dis Clin North Am. 2014 May;40(2):279-90. doi: 10.1016/j.rdc.2014.01.009. Epub 2014 Feb 19.

The genetic basis of gout.

Author information

1
Department of Biochemistry, University of Otago, Dunedin 9012, New Zealand. Electronic address: tony.merriman@otago.ac.nz.
2
Section of Rheumatology and Clinical Epidemiology Unit, Boston University School of Medicine, Boston, MA 02118, USA.
3
Department of Medicine, University of Auckland, Auckland 1023, New Zealand.

Abstract

Gout results from deposition of monosodium urate (MSU) crystals. Elevated serum urate concentrations (hyperuricemia) are not sufficient for the development of disease. Genome-wide association studies (GWAS) have identified 28 loci controlling serum urate levels. The largest genetic effects are seen in genes involved in the renal excretion of uric acid, with others being involved in glycolysis. Whereas much is understood about the genetic control of serum urate levels, little is known about the genetic control of inflammatory responses to MSU crystals. Extending knowledge in this area depends on recruitment of large, clinically ascertained gout sample sets suitable for GWAS.

KEYWORDS:

ABCG2; Association; Gene; Genome-wide association studies; Gout; SLC2A9; Urate

PMID:
24703347
DOI:
10.1016/j.rdc.2014.01.009
[Indexed for MEDLINE]
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