Elevated serum uric acid in nondiabetic people mark pro-inflammatory state and HDL dysfunction and independently predicts coronary disease

Onat A., Can G. , ORNEK E., Altay S., Yuksel M., Ademoglu E.

CLINICAL RHEUMATOLOGY, vol.32, no.12, pp.1767-1775, 2013 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 32 Issue: 12
  • Publication Date: 2013
  • Doi Number: 10.1007/s10067-013-2339-7
  • Title of Journal : CLINICAL RHEUMATOLOGY
  • Page Numbers: pp.1767-1775
  • Keywords: Coronary heart disease risk, HDL dysfunction, Metabolic syndrome, Pro-inflammatory state, Serum uric acid, HIGH-DENSITY-LIPOPROTEIN, METABOLIC SYNDROME, HEART-DISEASE, ARTERY-DISEASE, RISK, HYPERURICEMIA, MORTALITY, HYPERTENSION, METAANALYSIS, ALLOPURINOL


We explored the association of serum uric acid (UA) concentrations with pro-inflammatory state and high-density lipoprotein (HDL) dysfunction. UA tertiles in tracked 1,508 nondiabetic participants were analyzed cross-sectionally for associations with inflammation biomarkers and protective proteins over a mean follow-up of 4.9 years for incident coronary heart disease (CHD) using Cox proportional hazards regression. In the absence of metabolic syndrome (MetS), UA tertiles significantly distinguished, in each sex, increasing categories of three MetS components (inflammation/oxidation markers, apolipoprotein (apo)B) and (inversely) current smoking (but not protective proteins such as HDL, apoA-I, and adiponectin). Distinctions attenuated in the presence of MetS. Linear regression model revealed fasting triglycerides (1.86 mg/dl variance), male sex, and gamma-glutamyl transferase and age as covariates of UA levels in women. In Cox analysis, incident CHD (n = 137) was predicted by mid and upper UA tertile in men alone at significant hazard ratios of 2.7, additively to conventional risk factors. Elevated serum UA levels, linked to triglycerides, mark in nondiabetic people pro-inflammatory state, and, notably, HDL dysfunction. CHD risk is independently predicted by elevated UA levels in nondiabetic men and is modulated by MetS and gender.