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Rheumatology Advance Access originally published online on February 28, 2003
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Rheumatology 2003; 42: 468-472
© 2003 British Society for Rheumatology

The elevated prevalence of apolipoprotein E2 in patients with gout is associated with reduced renal excretion of urates

F. Cardona, F. J. Tinahones, E. Collantes1, A. Escudero1, E. García-Fuentes and F. J. Soriguer

Endocrinology and Nutrition Service, Pabellon 1 sotano Hospital Civil, Complejo hospitalario Carlos Haya, Plza del Hospital Civil s/n 29009 Málaga and
1 Servicio de Reumatologia, Hospital Reina Sofia Cordoba, Spain

Objective. Previous studies have demonstrated that the lower renal excretion of urates in patients with hyperuricaemia is inversely related to plasma very low-density lipoprotein (VLDL) levels, and the different genotypes of the apolipoprotein E gene are related to the plasma levels of lipids. The aim of this study was to determine the prevalence of apolipoprotein E in hyperuricaemic patients and to investigate whether the renal excretion of urates is conditioned by the apoliprotein E genotype.

Method. The plasma levels of lipoproteins, cholesterol, triglycerides and uric acid, and the renal excretion of uric acid were studied in 68 patients with gout and in another control group of 50 healthy subjects. Both groups were genotyped for apolipoprotein E by means of an amplification technique and inverse hybridization.

Results. The prevalence of the E2 allele was greater in the patients than in the control group. The levels of cholesterol, triglycerides and uric acid were greater in the patients, whereas the levels of high-density lipoprotein were lower. The patients with the E2 allele had higher levels of triglycerides in VLDL and intermediate-density lipoproteins and a lower renal excretion of urates.

Conclusions. These results show that the reduced renal excretion of uric acid in patients with gout is mediated by high levels of VLDL and by the high prevalence of the E2 allele of apolipoprotein E.

KEY WORDS: Apolipoprotein E, Gout, Hyperuricaemia.

Correspondence to: F. J. Tinahones. E-mail: labendo{at}hch.sas.cica.es


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