Flais Jérémy, Bardou-Jacquet Edouard, Deugnier Yves, Coiffier Guillaume, Perdriger Aleth, Chalès Gérard, Ropert Martine, Loréal Olivier, Guggenbuhl Pascal
Rheumatology Department, Rennes University Hospital, 16, bd de Bulgarie, 35203 Rennes, France.
INSERM UMR 991, 35000 Rennes, France; University Rennes 1, Medicine Faculty, 35043 Rennes, France; Reference Centre for Rare Genetic Iron Overload Disorders, Clinic for Liver Disorders, Rennes University Hospital, Pontchaillou Hospital, 2 rue Henri Le Guilloux, 35033 Rennes, France.
Joint Bone Spine. 2017 May;84(3):293-297. doi: 10.1016/j.jbspin.2016.05.020. Epub 2016 Sep 19.
Hyperuricemia is becoming increasingly frequent in the population, and is known to be sometimes the cause of gout. The impact of uric acid is still not clearly understood, however. The iron metabolism 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 patients who were homozygous for the HFE p.Cys282Tyr mutation.
738 patients with the HFE gene mutation Cys282Tyr in the homozygous state were included in the study. The variables measured during the initial evaluation were compared in univariate analysis by Student's t test. In multivariate analysis, linear stepwise regression was used.
In the group of hyperuricemic patients, ferritinemia was significantly higher than in the group of non-hyperuricemic patients (1576.7±1387.4μg/l vs. 1095.63±1319.24μg/l, P<0.005). With multivariate analysis, only ferritin and BMI independently explained the uricemia (R=0.258) after adjustment for age, glycemia and CRP. The correlation between uricemia and log(ferritin) with partial regression correlation coefficients was 0.307 (P<0.01).
The increase in uricemia is associated with the increase in ferritin in a population of patients who 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, could be a response to the visceral toxicity of excess non-transferrin bound iron linked to oxidative stress via the antioxidant properties of uric acid.
高尿酸血症在人群中越来越常见，并且已知有时是痛风的病因。然而，尿酸的影响仍未完全明确。铁代谢可能与尿酸代谢相互作用。本研究的目的是在一组HFE基因p.Cys282Tyr突变纯合的血色素沉着症患者中，研究血清尿酸水平与血清铁蛋白水平之间的关系。
本研究纳入了738例处于纯合状态的HFE基因突变Cys282Tyr患者。在初始评估期间测量的变量通过学生t检验进行单因素分析比较。在多因素分析中，使用线性逐步回归。
在高尿酸血症患者组中，铁蛋白血症显著高于非高尿酸血症患者组（1576.7±1387.4μg/l对1095.63±1319.24μg/l，P<0.005）。经过多因素分析，在调整年龄、血糖和CRP后，只有铁蛋白和BMI独立解释尿酸血症（R=0.258）。尿酸血症与log(铁蛋白)之间的偏回归相关系数为0.307（P<0.01）。
在HFE基因p.Cys282Tyr突变纯合的患者群体中，尿酸血症的增加与铁蛋白的增加相关，且独立于通常与高尿酸血症相关的因素。与高铁蛋白血症相关的尿酸增加，可能是对通过尿酸的抗氧化特性与氧化应激相关的非转铁蛋白结合铁过量的内脏毒性的一种反应。
