Hyperferritinemia increases the risk of hyperuricemia in HFE-hereditary hemochromatosis

International audienceObjectives: Hyperuricemia is becoming increasingly frequent in the population, and is known to besometimes the cause of gout. The impact of uric acid is still not clearly understood, however. The ironmetabolism may interact with the uric acid metabolism. The aim of this study was to examine the relationship between the serum uric acid and serum ferritin levels in a cohort of hemochromatosis patientswho were homozygous for the HFE p. Cys282Tyr mutation. Methods: 738 patients with the HFE gene mutation Cys282Tyr in the homozygous state were includedin the study. The variables measured during the initial evaluation were compared in univariate analysisby Student's t test. In multivariate analysis, linear stepwise regression was used. Results: In the group of hyperuricemic patients, ferritinemia was significantly higher than in the group ofnonhyperuricemic patients (1576.7 +/- 1387.4 mu g/l vs. 1095.63 +/- 1319.24 mu g/l, P < 0.005). With multivariate analysis, only ferritin and BMI independently explained the uricemia (R-2= 0.258) after adjustmentfor age, glycemia and CRP. The correlation between uricemia and log(ferritin) with partial regressioncorrelation coefficients was 0.307 (P < 0.01). Conclusions: The increase in uricemia is associated with the increase in ferritin in a population of patientswho were homozygous for the HFE gene mutation p. Cys282Tyr and this independently of factors commonly associated with hyperuricemia. The increase in uric acid associated with hyperferritinemia, couldbe a response to the visceral toxicity of excess non-transferrin bound iron linked to oxidative stress viathe antioxidant properties of uric acid. (C) 2016 Societe francaise de rhumatologie. Published by Elsevier Masson SAS. All rights reserved