Maqola

Uric acid and inflammatory markers

Carmelinda RuggieroLongitudinal Studies Section, Clinical Research Branch, National Institute on Aging, NIH, Baltimore, MD, USA. [email protected]Antonio CherubiniDepartment of Clinical and Experimental Medicine, Institute of Gerontology and Geriatrics, University of Perugia Medical School, Perugia, Italy;Alessandro BlèLongitudinal Studies Section, Clinical Research Branch, National Institute on Aging, NIH, Baltimore, MD, USA;Ângelo José Gonçalves BósLongitudinal Studies Section, Clinical Research Branch, National Institute on Aging, NIH, Baltimore, MD, USA;Marcello MaggioLongitudinal Studies Section, Clinical Research Branch, National Institute on Aging, NIH, Baltimore, MD, USA;Vishwa Deep DixitClinical Immunology Section, Laboratory of Immunology, National Institute on Aging, NIH, Baltimore, MD, USA;Fulvio LauretaniTuscany Regional Health Agency, Florence, Italy; andStefania BandinelliUmberto SeninDepartment of Clinical and Experimental Medicine, Institute of Gerontology and Geriatrics, University of Perugia Medical School, Perugia, Italy;Luigi FerrucciLongitudinal Studies Section, Clinical Research Branch, National Institute on Aging, NIH, Baltimore, MD, USA;

2006en

ABI

Annotatsiya

AIMS: 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. METHODS AND 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). CONCLUSION: 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.

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DOI: 10.1093/eurheartj/ehi879

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