4.7 Article

Serum urate is related to subclinical inflammation in asymptomatic hyperuricaemia

期刊

RHEUMATOLOGY
卷 60, 期 1, 页码 371-379

出版社

OXFORD UNIV PRESS
DOI: 10.1093/rheumatology/keaa425

关键词

asymptomatic hyperuricaemia; inflammation; cytokines; gene expression

资金

  1. Sociedad Espanola de Nefrologia (AYUSEN2015)
  2. ACINEF (ACNEF-2015)

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This study found that serum uric acid levels are associated with inflammation in asymptomatic hyperuricaemia (AHU) patients, and UA levels may be an inducer of subclinical inflammation. Therapeutic reduction of UA levels was associated with modulation of inflammatory characteristics.
Objective. Asymptomatic hyperuricaemia (AHU) is associated with inflammatory disorders, including cardiovascular disease. Uric acid (UA) lowering therapies may reduce the risk of appearance or the progression of these comorbidities. In this work, we investigated the relationship between serum UA levels and inflammation in subjects with AHU. Methods. Serum levels of high-sensitivity CRP (hsCRP), TNF-alpha and IL-6, and mRNA expression of TNFa and IL6 in peripheral blood mononuclear cells were measured in individuals with AHU and without comorbid conditions and in a control group with similar characteristics and normal serum UA levels. Additionally, we determined the variations in the inflammatory profile in a subgroup of subjects after 6 months of treatment with allopurinol. Results. Subjects at higher tertiles of serum UA presented higher levels of hsCRP and increased serum and mRNA expression levels of both cytokines (P < 0.001). UA levels constituted an independent predictor of increased levels of inflammatory parameters in multiple regression models (P <0.001) and a risk factor for the presence of a subclinical inflammation in multivariate logistic regression (P <0.001). Allopurinol reduced UA and serum and mRNA expression of inflammatory cytokines (P< 0.001). There was a significant correlation between the variations in serum UA and the variations in serum TNF-alpha (P <0.01) and IL-6 (P <0.05), and mRNA expression of these cytokines (P <0.05). This association remained significant and independent (P <0.01). Conclusion. In subjects with AHU, serum UA may be an inductor of subclinical inflammation. Therapeutic reduction of serum UA was associated with a modulation of the inflammatory profile.

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