Uric acid: A marker of increased cardiovascular risk
Lipid Clinic Heart Institute (InCor), University of Sao Paulo Medical School Hospital, Sao Paulo, Brazil. Atherosclerosis
(Impact Factor: 3.99).
06/2008; 202(1):11-7. DOI: 10.1016/j.atherosclerosis.2008.05.022
The relationship between uric acid and cardiovascular disease has been known since the 19th century, after that many authors reported the classical association of gout, hypertension, obesity and cardiovascular disease. With the exception of specific genetic defects in purine metabolism, increased uric acid is generally associated with important risk factors for atherosclerosis like hypertension, abdominal obesity, insulin resistance, the metabolic syndrome and renal failure. Studies have clearly shown an association between increased uric acid concentrations with oxidative stress, endothelial dysfunction, inflammation, subclinical atherosclerosis and an increased risk of cardiovascular events. Increased uric acid levels are independent markers of cardiovascular disease risk. Prospective studies are necessary to show that reduction of uric acid levels prevent cardiovascular events.
Available from: Yuegang Zuo
- "Their concentrations may affect human health and act as biomarkers for various diseases (Ascherio et al., 2009; Burtis & Ashwood, 2001; Choi, Mount, & Reginato, 2005; Chonchol et al., 2007; Dehghan, van Hoek, Sijbrands, Hofman, & Witteman, 2008; Gagliardi, Miname, & Santos, 2009; Harper, 1977; Heinig & Johnson, 2006; Kassirer, 1971; Krishnan, Kwoh, Schumarcher, & Kuller, 2007; Lapsia et al., 2012; Lin et al., 2011; Mouton & Holder, 2006). The abnormal high concentrations of uric acid in human plasma and urine are associated with several diseases, such as gouty arthritis, hyperuricemia, hypertension, pneumonia, type 2 diabetes, cardiovascular disease and kidney damage (Ascherio et al., 2009; Burtis & Ashwood, 2001; Choi et al., 2005; Chonchol et al., 2007; Dehghan et al., 2008; Gagliardi et al., 2009; Harper, 1977; Heinig & Johnson, 2006; Kassirer, 1971; Krishnan et al., 2007; Lapsia et al., 2012; Lin et al., 2011; Mouton & Holder, 2006). Creatinine, quantitatively excreted in the urine, is nonenzymatically formed from intracellular creatine and phosphocreatine in muscles. "
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ABSTRACT: Creatinine (Cr), uric (UA) and ascorbic acid (AA) are common constituents in human fluids. Their abnormal concentrations in human fluids are associated with various diseases. Thus, apart from the endogenous formation in human body, it is also important to examine their sources from food products. In this study, a rapid and accurate HILIC method was developed for simultaneous determination of Cr, UA and AA in bovine milk and orange juice. Milk samples were pretreated by protein precipitation, centrifugation and filtration, followed by HPLC separation and quantification using a Waters Spherisorb S5NH2 column. The developed method has been successfully applied to determine the concentration of UA, AA and Cr in milk and fruit juice samples. The milk samples tested were found to contain UA and creatinine in the concentration range of 24.1-86.0 and 5.07-11.2μgmL(-1), respectively. The orange juices contain AA over 212μgmL(-1).
Copyright © 2015 Elsevier Ltd. All rights reserved.
Food Chemistry 09/2015; 182. DOI:10.1016/j.foodchem.2015.02.142 · 3.39 Impact Factor
Available from: Emilio Ros
- "It has been suggested that it might be secondary to an association with obesity, insulin resistance, and dyslipidemia, which are associated with an inflammatory state. Some authors have suggested that uric acid has pro-inflammatory effects because it stimulates several inflammatory molecules . It is known that the pro-inflammatory state precedes MetS development and Figure 1 Cox regression models for assessing the relative risk of metabolic syndrome and the incidence of its features by sex-adjusted SUA quartiles (Q1 versus Q4). "
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ABSTRACT: Background and aims:
Several studies have demonstrated a relationship between increased serum uric acid (SUA) concentrations and the prevalence of metabolic syndrome (MetS) in the oriental population. However, to the best of our knowledge, the association between SUA and MetS has never been investigated in elderly European individuals at high cardiovascular risk. The aim of this study was to conduct a cross-sectional and prospective evaluation of the associations between SUA concentrations and the MetS in elderly individuals at high cardiovascular risk.
Methods and results:
Men and women (55-80 years of age) from different PREDIMED (Prevención con DIeta MEDiterránea) recruiting centers were studied. Baseline cross-sectional (n = 4417) and prospective assessments (n = 1511) were performed. MetS was defined in accordance with the updated harmonized criteria. Anthropometric measurements and biochemical determinations were assessed at baseline and yearly during follow-up. Unadjusted and adjusted regression models were fitted to assess the risk of MetS and its components according to the levels of baseline SUA. Participants in the highest baseline sex-adjusted SUA quartile showed an increased prevalence of MetS than those in the lowest quartile, even after adjusting for potential confounders (odd ratio (OR): 2.3 (95% confidence interval (CI), 1.8-2.8); P < 0.001). Participants in the highest baseline sex-adjusted SUA quartile presented a higher incidence of new-onset MetS than those in the lowest quartile (hazard ratios (HR): 1.4 (95% CI, 1.1-1.9); P < 0.001). Participants initially free at baseline of hypertriglyceridemia (HR: 1.9 (1.6-2.4); P < 0.001), low high-density lipoprotein (HDL)-cholesterol (HR: 1.4 (1.1-1.7); P = 0.002), and hypertension components of MetS (HR: 2.0 (1.2-3.3); P = 0.008) and who were in the upper quartile of SUA had a significantly higher risk of developing these MetS components during follow-up.
Elevated SUA concentrations are significantly associated with the development of MetS.
Nutrition Metabolism and Cardiovascular Diseases 10/2014; 25(2). DOI:10.1016/j.numecd.2014.10.006 · 3.32 Impact Factor
Available from: Harald E Vonkeman
- "There are different pathophysiologic hypotheses that may explain the observed associations: shared risk factors, direct metabolic actions of uric acid on the vascular wall and/or on renin-angiotensin-aldosterone and insulin resistance pathways, or vascular involvement in systemic inflammatory activation. Even though all of these hypotheses are supported by experimental and/or epidemiologic data, none has been definitely confirmed [18,19]. Causality in gout associated cardiovascular risk thus remains unelucidated and pathways are probably complex. "
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Gout and hyperuricaemia may be associated with increased cardiovascular risk, but analyses in different populations show conflicting results. This study investigates the impact of serum uric acid, inflammation and traditional CV risk parameters on CV event risk in patients with gouty arthritis and patients with non-gouty rheumatic disease.
cross-sectional and prospective multivariate analysis of the relation between tertiles of serum uric acid and individual traditional CV risk factors in a cohort of gouty arthritis (GA, n=172), rheumatoid arthritis (RA, n=480) and osteoarthritis (OA, n=206) patients. Main outcome measures: systolic blood pressure, TC/HDL ratio, GlyHb, BMI and first CV events.
Individual CV risk factors were significantly less favourable in GA (systolic blood pressure, TC/HDL ratio, BMI, p<0.05). In RA and OA, but not in GA, individual cardiometabolic parameters correlated with serum uric acid values (OA: RA: systolic blood pressure, TC/HDL ratio, BMI; systolic blood pressure, TC/HDL ratio, GlyHb, BMI; p<0.05). In non-GA individuals the highest tertile of serum uric acid (>0.34 mmol/L) and NT proBNP level were independent predictors of first CV events, against age and GlyHb level in GA (p<0.05). The hazard of first CV events was equally significantly increased in GA patients (HR 3.169, 95% CI 1.287-7.806) and non-GA individuals with a serum uric acid ≥ 0.34 mmol/L (HR 3.721, 95% CI 1.603-8.634) compared to non-GA individuals with a serum uric acid < 0.27.
GA is associated with a 3.1-fold hazard of first CV events. In non-GA rheumatic patients increasing serum uric acid is associated with increased CV risk, whereas CV risk in GA is independent of serum uric acid values. The presence of GA or a baseline serum uric acid in the upper range are possibly stronger predictors of first CV events than some traditional CV risk factors or parameters of inflammation.
BMC Musculoskeletal Disorders 05/2014; 15(1):174. DOI:10.1186/1471-2474-15-174 · 1.72 Impact Factor
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