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      Prevalence of high serum uric acid is increased in ambulatory subjects with hyperglycemia and dyslipidemia Translated title: A prevalência de hiperuricemia está aumentada em pacientes ambulatoriais com hiperglicemia e dislipidemia

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          Abstract

          INTRODUCTION: Serum uric acid has been considered a marker or an element of the clinical and laboratory alterations in the metabolic syndrome. OBJECTIVE: to evaluate the association between levels of serum uric acid (UA) and the following laboratory profile: fasting glucose > 100 mg/dl, triglycerides > 150 mg/dl and high density lipoprotein cholesterol (HDL-C) < 50 mg/dl in women and < 40 mg/dl in men. METHOD: In a cross-sectional survey, blood samples of 4,328 randomized outpatients aged from 20 to 102 years were analyzed. RESULTS: The mean (interquartile range) UA level was higher in men (6.7; 2.4-12.5 mg/dl) and women (5.4; 2.0-12.2 mg/dl) with the laboratorial profile than in those without it (5.9; 0.90-33.8 mg/dl for men and 4.4; 0.8-30.0 mg/dl for women) (p < 0.0001). A significant increase in the prevalence of laboratory profile was observed in men (OR = 2.2 mg/dl; 95% CI: 1.2-3.9 mg/dl) and women (OR = 2.2 mg/dl; 95% CI: 1.4-3.5 mg/dl) with hyperuricemia. CONCLUSION: These results show the association between serum levels of uric acid and metabolic syndrome profile, which corroborates to similar results found in other populations worldwide.

          Translated abstract

          INTRODUÇÃO: O ácido úrico sérico tem sido considerado um marcador ou componente das alterações clínicas e laboratoriais da síndrome metabólica. OBJETIVO: Avaliar a associação entre o ácido úrico sérico (AU) e o perfil laboratorial composto de glicemia de jejum > 100 mg/dl, triglicerídeos > 150 mg/dl e colesterol da lipoproteína de alta densidade (HDL-C) < 50 mg/dl nas mulheres e < 40 mg/dl nos homens. MÉTODO: Em estudo de corte transversal, amostras de sangue de 4.328 pacientes ambulatoriais não selecionados com idade variando de 20 a 102 anos foram examinadas. RESULTADOS: A mediana (variação interquartil) do AU foi mais elevada nos homens (6,7; 2,4-12,5 mg/dl) e mulheres (5,4;2-12,2 mg/dl) que apresentaram o perfil laboratorial do que nos que não o apresentaram (5,9; 0,9-33,8 mg/dl para os homens e 4,4; 0,8-30 mg/dl para as mulheres) (p < 0,0001). Observou-se aumento significativo na prevalência do perfil laboratorial nos homens (razão de chance [RC] = 2,2 mg/dl; intervalo de confiança [IC] 95%: 1,2-3,9 mg/dl) e mulheres (RC = 2,2 mg/dl; IC 95%: 1,4-3,5 mg/dl) com hiperuricemia. CONCLUSÃO: Esses resultados mostram a associação dos níveis séricos do acido úrico com o perfil laboratorial da síndrome metabólica nesse grupo não selecionado de indivíduos brasileiros atendidos ambulatorialmente, sendo este um achado semelhante ao observado em outras populações estudadas mundialmente.

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          Most cited references 22

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          A causal role for uric acid in fructose-induced metabolic syndrome.

          The worldwide epidemic of metabolic syndrome correlates with an elevation in serum uric acid as well as a marked increase in total fructose intake (in the form of table sugar and high-fructose corn syrup). Fructose raises uric acid, and the latter inhibits nitric oxide bioavailability. Because insulin requires nitric oxide to stimulate glucose uptake, we hypothesized that fructose-induced hyperuricemia may have a pathogenic role in metabolic syndrome. Four sets of experiments were performed. First, pair-feeding studies showed that fructose, and not dextrose, induced features (hyperinsulinemia, hypertriglyceridemia, and hyperuricemia) of metabolic syndrome. Second, in rats receiving a high-fructose diet, the lowering of uric acid with either allopurinol (a xanthine oxidase inhibitor) or benzbromarone (a uricosuric agent) was able to prevent or reverse features of metabolic syndrome. In particular, the administration of allopurinol prophylactically prevented fructose-induced hyperinsulinemia (272.3 vs.160.8 pmol/l, P < 0.05), systolic hypertension (142 vs. 133 mmHg, P < 0.05), hypertriglyceridemia (233.7 vs. 65.4 mg/dl, P < 0.01), and weight gain (455 vs. 425 g, P < 0.05) at 8 wk. Neither allopurinol nor benzbromarone affected dietary intake of control diet in rats. Finally, uric acid dose dependently inhibited endothelial function as manifested by a reduced vasodilatory response of aortic artery rings to acetylcholine. These data provide the first evidence that uric acid may be a cause of metabolic syndrome, possibly due to its ability to inhibit endothelial function. Fructose may have a major role in the epidemic of metabolic syndrome and obesity due to its ability to raise uric acid.
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            Use of allopurinol in slowing the progression of renal disease through its ability to lower serum uric acid level.

            Hyperuricemia is associated strongly with the development of hypertension, renal disease, and progression. Allopurinol decreases serum uric acid levels by inhibiting the enzyme xanthine oxidase. We hypothesized that administrating allopurinol to decrease serum uric acid levels to the normal range in hyperuricemic patients with chronic kidney disease may be of benefit in decreasing blood pressure and slowing the rate of renal disease progression in these patients. We conducted a prospective, randomized, controlled trial of 54 hyperuricemic patients with chronic kidney disease. Patients were randomly assigned to treatment with allopurinol, 100 to 300 mg/d, or to continue the usual therapy for 12 months. Clinical, hematologic, and biochemical parameters were measured at baseline and 3, 6, and 12 months of treatment. We define our study end points as: (1) stable kidney function with less than 40% increase in serum creatinine level, (2) impaired renal function with creatinine level increase greater than 40% of baseline value, (3) initiation of dialysis therapy, and (4) death. One patient in the treatment group dropped out because of skin allergy to allopurinol. Serum uric acid levels were significantly decreased in subjects treated with allopurinol, from 9.75 +/- 1.18 mg/dL (0.58 +/- 0.07 mmol/L) to 5.88 +/- 1.01 mg/dL (0.35 +/- 0.06 mmol/L; P < 0.001). There were no significant differences in systolic or diastolic blood pressure at the end of the study comparing the 2 groups. There was a trend toward a lower serum creatinine level in the treatment group compared with controls after 12 months of therapy, although it did not reach statistical significance (P = 0.08). Overall, 4 of 25 patients (16%) in the allopurinol group reached the combined end points of significant deterioration in renal function and dialysis dependence compared with 12 of 26 patients (46.1%) in the control group (P = 0.015). Allopurinol therapy significantly decreases serum uric acid levels in hyperuricemic patients with mild to moderate chronic kidney disease. Its use is safe and helps preserve kidney function during 12 months of therapy compared with controls. Results of this study need to be confirmed with an additional prospective trial involving a larger cohort of patients to determine the long-term efficacy of allopurinol therapy and in specific chronic kidney disease subpopulations.
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              Established risk factors and coronary artery disease: the Framingham Study.

               Steven Wilson (1994)
              Long-standing risk factors for the development of coronary artery disease (CAD) have typically included age, blood levels of total and high-density lipoprotein (HDL) cholesterol, blood pressure, cigarette use, diabetes mellitus, and left ventricular hypertrophy on electrocardiography. Each of the traditional risk-factor measures has expanded in scope over time; for instance, systolic and diastolic blood pressure levels are each associated with the occurrence of CAD, and an individual need not be hypertensive to be at an increased risk. Although total (or low-density lipoprotein cholesterol) and HDL cholesterol are highly associated with CAD incidence, other newer lipid measures such as apolipoproteins A-I and B, and genetic markers have shown little or no additional effect in predicting CAD. Diabetes mellitus has been consistently associated with CAD but less data are available to demonstrate independent roles for obesity and regional adiposity. Although reports are more recent, hematologic factors such as fibrinogen concentration and leukocyte count have been consistently associated with CAD in observational studies. Prediction equations continue to emphasize the traditional biological factors and not behaviors. Among life-style habits such as diet, sedentary activity, and cigarette smoking, only the latter has been consistently used in CAD prediction because of its independent effect.
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                jbpml
                Jornal Brasileiro de Patologia e Medicina Laboratorial
                J. Bras. Patol. Med. Lab.
                Sociedade Brasileira de Patologia Clínica (Rio de Janeiro )
                1678-4774
                August 2010
                : 46
                : 4
                : 283-288
                Affiliations
                [1 ] Universidade de Brasília Brazil
                [2 ] Universidade de Brasília Brazil
                [3 ] Universidade de Brasília Brazil
                [4 ] Universidade de Brasília Brazil
                Article
                S1676-24442010000400004
                10.1590/S1676-24442010000400004
                Product
                Product Information: website
                Categories
                MEDICAL LABORATORY TECHNOLOGY
                MEDICINE, RESEARCH & EXPERIMENTAL
                PATHOLOGY

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