Does diagnosis of metabolic syndrome predict the likelihood of peripheral arterial disease as defined by a low ankle-brachial index?

BACKGROUND: There is limited information about whether a diagnosis of metabolic syndrome (MS) predicts peripheral arterial disease independently of diabetes. This study assessed whether MS adds prognostic information beyond that relating to diabetes in the identification of a low ankle-brachial index (ABI). DESIGN: Cross-sectional population-based study of people aged 50-75 years. METHODS: Eight hundred and fifty-eight participants were randomly selected. The likelihood of low ABI (<0.90) was calculated according to MS status before and after excluding diabetes. The National Cholesterol Education Panel and the International Diabetes Federation (IDF) definitions of MS were used. RESULTS: The prevalence of National Cholesterol Education Panel-defined and IDF-defined MS, and low ABI was 57.8, 61.1 and 7.5%, respectively. When there were participants with three or more criteria for MS, participants with only three criteria, and participants with four or five criteria were compared with participants without MS, the odds ratio for low ABI was 1.89 (95% confidence interval, 1.08-3.30), 1.34 (0.70-2.60) and 2.70 (1.45-5.03), respectively. The association of MS and low ABI lost statistical significance after excluding diabetes. No difference was observed using the IDF definition of MS. CONCLUSION: Screening of participants with MS does not improve the identification of abnormal ABI provided by diabetes.

[Serum urate levels and urinary uric acid excretion in subjects with metabolic syndrome]. / Concentraciones séricas de uratos y excreción urinaria de ácido úrico en individuos con síndrome metabólico.

BACKGROUND AND OBJECTIVES: Hyperuricemia is considered a feature of the metabolic syndrome (MS) despite serum uric acid (SUA) is not considered a diagnostic criterion. The main physiopathological disturbance leading to the increased SUA is not completely understood. PATIENTS AND METHOD: Descriptive study without drug intervention including 141 subjects (NCEP-ATPIII: 105 with MS and 36 without MS). Serum UA levels were compared in subjects with and without MS. The mechanism of the rise in SUA levels was assessed (overproduction or decreased renal excretion). The relation of SUA levels to the HOMA index was also evaluated. RESULTS: Subjects with MS showed significantly higher SUA levels (5.6 [1.6] vs 4.6 [1.7] mg/dl, p = 0.002), and lower urinary UA excretion than subjects without MS (UA clearance 3.60 [2.41] vs 4.65 [3.04] ml/min/m2, p = 0.049; excreted fraction of filtered UA 7.15 [4.72] vs 9.81 [6.78%], p = 0.045). Sex (male 6.1 [1.6] vs female 4.9 [1.6] mg/dl, p < 0.001), alcohol intake (drinkers 6.1 [1.8] vs non-drinkers 5.2 [1.6] mg/dl, p < 0.01), and MS (present 5.6 [1.6] absent 4.6 [1.7] mg/dl, p < 0.002), were significantly associated with SUA. In the multiple regression analysis, sex and MS were independently associated with SUA. CONCLUSIONS: This study demonstrates significantly higher SUA levels in subjects with MS. A decreased urinary UA excretion, instead of urate overproduction, was the leading mechanism to explain high SUA. Serum UA levels were not associated with the HOMA index.

Concentraciones séricas de uratos y excreción urinaria de ácido úrico en individuos con síndrome metabólico / Serum urate levels and urinary uric acid excretion in subjects with metabolic syndrome

Fundamento y objetivos: La hiperuricemia es una de las alteraciones características del síndrome metabólico (SM), aunque no incluida como criterio diagnóstico. No se conoce con exactitud el mecanismo que causa la elevación del urato sérico en el SM. Pacientes y método: Estudio transversal, sin intervención farmacológica, sobre 141 individuos (National Cholesterol Education Program Adult Treatment Panel III: 105 con SM y 36 sin SM). Se comparan los valores de urato sérico entre individuos con y sin SM, y se analiza si la elevación del urato sérico se asocia a infraexcreción renal o sobreproducción. Se determina la asociación del urato sérico a índice HOMA. Resultados: El grupo con SM presentó valores de urato sérico significativamente más elevados (media [DE] 5,6 [1,6] frente a 4,6 [1,7] mg/dl, p = 0,002), y menor excreción urinaria (aclaramiento de ácido úrico 3,60 [2,41] frente a 4,65 [3,04] ml/min/m2, p = 0,049; fracción excretada del ácido úrico filtrado 7,15 [4,72] frente a 9,81 [6,78]%, p = 0,045). Las variables asociadas con los valores de urato sérico fueron el sexo (media de urato sérico en varón 6,1 [1,6] frente a mujer 4,9 [1,6] mg/dl, p < 0,001), el alcohol (bebedores 6,1 [1,8] frente a no bebedores 5,2 [1,6] mg/dl, p < 0,01), y el SM (presente 5,6 [1,6] frente a ausente 4,6 [1,7] mg/dl, p < 0,002). En el análisis multivariante, sólo el sexo y el SM se asociaron independientemente con los valores de urato sérico. Conclusiones: El presente estudio muestra unos valores de urato sérico significativamente más elevados entre individuos con SM, relacionado a su vez con una infraexcreción renal de uratos. No se observó asociación significativa de los valores de urato sérico con el índice HOMA

Background and objectives: Hyperuricemia is considered a feature of the metabolic syndrome (MS) despite serum uric acid (SUA) is not considered a diagnostic criterion. The main physiopathological disturbance leading to the increased SUA is not completely understood. Patients and method: Descriptive study without drug intervention including 141 subjects (NCEP-ATPIII: 105 with MS and 36 without MS). Serum UA levels were compared in subjects with and without MS. The mechanism of the rise in SUA levels was assessed (overproduction or decreased renal excretion). The relation of SUA levels to the HOMA index was also evaluated. Results: Subjects with MS showed significantly higher SUA levels (5.6 [1.6] vs 4.6 [1.7] mg/dl, p = 0.002), and lower urinary UA excretion than subjects without MS (UA clearance 3.60 [2.41] vs 4.65 [3.04] ml/min/m2, p = 0.049; excreted fraction of filtered UA 7.15 [4.72] vs 9.81 [6.78%], p = 0.045). Sex (male 6.1 [1.6] vs female 4.9 [1.6] mg/dl, p < 0.001), alcohol intake (drinkers 6.1 [1.8] vs non-drinkers 5.2 [1.6] mg/dl, p < 0.01), and MS (present 5.6 [1.6] absent 4.6 [1.7] mg/dl, p < 0.002), were significantly associated with SUA. In the multiple regression analysis, sex and MS were independently associated with SUA. Conclusions: This study demonstrates significantly higher SUA levels in subjects with MS. A decreased urinary UA excretion, instead of urate overproduction, was the leading mechanism to explain high SUA. Serum UA levels were not associated with the HOMA index