title: Uric acid and inflammatory markers.
abstract: OBJECTIVE
  The role of uric acid (UA) in the process of atherosclerosis and atherotrombosis is controversial. Epidemiological studies have recently shown that UA may be a risk factor for cardiovascular diseases and a negative prognostic marker for mortality in subjects with pre-existing heart failure.
  
  
  RESULTS
  We evaluate a relationship between UA levels and several inflammatory markers in 957 subjects, free of severe renal failure, from a representative Italian cohort of persons aged 65-95. Plasma levels of UA and white blood cell (WBC) and neutrophil count, C-reactive protein, interleukin-1 receptor antagonist (IL-1ra), interleukin-6 (IL-6), soluble IL-6 receptor (sIL-6r), interleukin-18 (IL-18), and tumor necrosis factor-alpha (TNF-alpha) were measured. Complete information on potential confounders was collected using standard methods. WBC (P=0.0001), neutrophils (P<0.0001), C-reactive protein (P<0.0001), IL-1ra (P<0.0001), IL-6 (P=0.0004), sIL-6r (P=0.002), IL-18 (P<0.0001), TNF-alpha (P=0.0008), and the percentage of subjects with abnormally high levels of C-reactive protein (P=0.004) and IL-6 (P=<0.0001) were significantly higher across UA quintiles. After adjustment for age, sex, behaviour- and disease-related confounders, results were virtually unchanged. In subjects with UA within the normal range, UA was significantly and independently associated with neutrophils count, C-reactive protein, IL-6, IL-1ra, IL-18, and TNF-alpha, whereas non-significant trends were observed for WBC (P=0.1) and sIL-6r (P=0.2).
  
  
  CONCLUSIONS
  A positive and significant association between UA and several inflammatory markers was found in a large population-based sample of older persons and in a sub-sample of participants with normal UA. Accordingly, the prevalence of abnormally high levels of C-reactive protein and IL-6 increased significantly across UA quintiles.
authors.affiliation: Longitudinal Studies Section, Clinical Research Branch, National Institute on Aging, NIH, Baltimore, MD, USA. ruggieroc@grc.nih.gov
authors.forename: Carmelinda
authors.initials: C
authors.lastname: Ruggiero
authors.forename: Antonio
authors.initials: A
authors.lastname: Cherubini
authors.forename: Alessandro
authors.initials: A
authors.lastname: Ble
authors.forename: Angelo J G
authors.initials: AJ
authors.lastname: Bos
authors.forename: Marcello
authors.initials: M
authors.lastname: Maggio
authors.forename: Vishwa D
authors.initials: VD
authors.lastname: Dixit
authors.forename: Fulvio
authors.initials: F
authors.lastname: Lauretani
authors.forename: Stefania
authors.initials: S
authors.lastname: Bandinelli
authors.forename: Umberto
authors.initials: U
authors.lastname: Senin
authors.forename: Luigi
authors.initials: L
authors.lastname: Ferrucci
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D050197:Atherosclerosis / Q000097:blood / Q000209:etiology*; D015415:Biomarkers / Q000097:blood*; D002097:C-Reactive Protein / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D005260:Female; D006801:Humans; D007958:Leukocyte Count; D007962:Leukocytes; D008297:Male; D009504:Neutrophils; D012307:Risk Factors; D013927:Thrombosis / Q000097:blood / Q000209:etiology*; D014527:Uric Acid / Q000378:metabolism*
chemical_list: D015415:Biomarkers; D016207:Cytokines; D014527:Uric Acid; D002097:C-Reactive Protein