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.
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.
Authors: Fredrik Nyberg; Laura Horne; Robert Morlock; Javier Nuevo; Chris Storgard; Lalitha Aiyer; Dionne M Hines; Xavier Ansolabehere; Pierre Chevalier Journal: Adv Ther Date: 2016-05-26 Impact factor: 3.845