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Effect of Apolipoprotein E Polymorphism on Serum Uric Acid Levels in Healthy Subjects
  1. Evagelos N. Liberopoulos,
  2. George A. Miltiadous,
  3. Vasilios G. Athyros,
  4. Manolis Ganotakis,
  5. Marios Cariolou,
  6. Eleni Bairaktari,
  7. Moses S. Elisaf
  1. Presented in part at the XV International Symposium on Drugs Affecting Lipid Metabolism, Venice, Italy, October 24-27, 2004.
  1. Address correspondence to: Dr. Moses S. Elisaf, Department of Internal Medicine, University of Ioannina, 451 10 Ioannina, Greece; e-mail: egepi{at}
  2. From the Department of Internal Medicine (E.N.L., G.A.M., M.S.E.) and Laboratory of Biological Chemistry (E.B.), School of Medicine, University of Ioannina, Ioannina, Greece; Atherosclerosis Unit (V.G.A.), Aristotelian University, Hipocration Hospital, Thessaloniki, Greece; Department of Internal Medicine (M.G.), School of Medicine, University of Crete, Heraklion, Greece; Molecular Genetics Department B-DNA Identification Laboratory (M.C.), Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus.


Background We have previously shown that apolipoprotein E (apo E-) polymorphism may affect serum creatinine concentration and predicted glomerular filtration rate in healthy individuals. On the other hand, there are limited data regarding the possible influence of apo E- polymorphism on serum uric acid (SUA) levels.

Methods Two hundred ninety (148 male, 142 female) apparently healthy white individuals were studied. apo E- genotypes, serum lipid parameters including apolipoproteins, insulin resistance using the homeostasis model assessment (HOMA) as a marker, serum and urine creatinine levels, and serum and urine uric acid concentration were determined in all participants.

Results The apo E-2 allele was associated with lower serum levels of total cholesterol, higher levels of triglycerides and apo E-, and increased serum creatinine concentration compared with the apo E-3 and apo E-4 alleles in our population. Furthermore, the apo E-2 allele was associated with higher SUA levels (321.3 ± 101.1 μmol/L [5.4 ± 1.7 mg/dL]) compared with the apo E-3 allele (261.8 ± 89.2 μmol/L [4.4 ± 1.5 mg/dL]; p = .012) and the apo E-4 allele (243.9 ± 65.4 μmol/L [4.1 ± 1.1 mg/dL]; p = .010), whereas the apo E-2 allele was associated with a nonsignificant decrease in the fractional renal excretion of uric acid (FEUA) compared with the apo E-3 and apo E-4 alleles (7.9 ± 2.2% vs 8.7 ± 4.2% vs 8.9 ± 5.1%, respectively; p = .53). These observations remained statistically significant when the effect of apo E- polymorphism on SUA levels was adjusted for gender, age, systolic and diastolic blood pressure, body mass index, serum creatinine, and triglyceride and apo E- levels, as well as for HOMA index and FEUA.

Conclusions Our data provide evidence, for the first time, that the apo E-2 allele is independently associated with increased SUA levels in healthy individuals.

Key Words
  • apolipoprotein E
  • uric acid
  • lipid metabolism

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