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代谢综合征患者的血清尿酸水平与尿尿酸排泄

[Serum urate levels and urinary uric acid excretion in subjects with metabolic syndrome].

作者信息

López-Suárez Alejandro, Elvira-González Javier, Bascuñana-Quirell Antonio, Rosal-Obrador Joan, Michán-Doña Alfredo, Escribano-Serrano José, Benítez-Rodríguez Encarnación

机构信息

Servicio de Medicina Interna, Hospital Virgen del Camino, Sanlúcar de Barrameda, Cádiz, Spain.

出版信息

Med Clin (Barc). 2006 Mar 11;126(9):321-4. doi: 10.1157/13085753.

DOI:10.1157/13085753
PMID:16650362
Abstract

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.

摘要

背景与目的

尽管血清尿酸(SUA)不被视为代谢综合征(MS)的诊断标准,但高尿酸血症被认为是代谢综合征的一个特征。导致SUA升高的主要生理病理紊乱尚未完全明确。

患者与方法

无药物干预的描述性研究,纳入141名受试者(美国国家胆固醇教育计划成人治疗组第三次报告[ NCEP-ATPIII ]标准:105名患有MS,36名未患MS)。比较了患有和未患有MS的受试者的血清尿酸水平。评估了SUA水平升高的机制(尿酸生成过多或肾脏排泄减少)。还评估了SUA水平与胰岛素抵抗稳态模型评估指数(HOMA指数)的关系。

结果

患有MS的受试者SUA水平显著更高(5.6 [1.6] 对比 4.6 [1.7] mg/dl,p = 0.002),且尿尿酸排泄低于未患MS的受试者(尿酸清除率3.60 [2.41] 对比 4.65 [3.04] ml/min/m²,p = 0.049;滤过尿酸排泄分数7.15 [4.72] 对比 9.81 [6.78%],p = 0.045)。性别(男性6.1 [1.6] 对比女性4.9 [1.6] mg/dl,p < 0.001)、饮酒情况(饮酒者6.1 [1.8] 对比不饮酒者5.2 [1.6] mg/dl,p < 0.01)以及MS(存在5.6 [1.6] 不存在4.6 [1.7] mg/dl,p < 0.002)均与SUA显著相关。在多元回归分析中,性别和MS与SUA独立相关。

结论

本研究表明患有MS的受试者SUA水平显著更高。尿尿酸排泄减少而非尿酸生成过多是导致高SUA的主要机制。血清尿酸水平与HOMA指数无关。

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