Prevalence of the metabolic syndrome in individuals with hyperuricemia

被引:586
作者
Choi, Hyon K.
Ford, Earl S.
机构
[1] Univ British Columbia, Vancouver Gen Hosp, Div Rheumatol, Arthrit Res Ctr Canada,Dept Med, Vancouver, BC V5Z 1L7, Canada
[2] Brigham & Womens Hosp, Channing Lab, Div Renal, Dept Med, Boston, MA 02115 USA
[3] Ctr Dis Control & Prevent, Div Adult & Community Hlth, Atlanta, GA USA
关键词
hypertension; insulin resistance; metabolic syndrome; NHANES III; obesity; uric acid;
D O I
10.1016/j.amjmed.2006.06.040
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
PURPOSE: The link between hyperuricemia and insulin resistance has been noted, but the prevalence of the metabolic syndrome by recent definitions among individuals with hyperuricemia remains unclear. Our objective was to determine the prevalence of the metabolic syndrome according to serum uric acid levels in a nationally representative sample of US adults. METHODS: By using data from 8669 participants aged 20 years and more in The Third National Health and Nutrition Examination Survey ( 1988- 1994), we determined the prevalence of the metabolic syndrome at different serum uric acid levels. We used both the revised and original National Cholesterol Education Program Adult Treatment Panel ( NCEP/ ATP) III criteria to define the metabolic syndrome. RESULTS: The prevalences of the metabolic syndrome according to the revised NCEP/ ATP III criteria were 18.9% ( 95% confidence interval [ CI], 16.8- 21.0) for uric acid levels less than 6 mg/ dL, 36.0% ( 95% CI, 32.5- 39.6) for uric acid levels from 6 to 6.9 mg/ dL, 40.8% ( 95% CI, 35.3- 46.4) for uric acid levels from 7 to 7.9 mg/ dL, 59.7% ( 95% CI, 53.0- 66.4) for uric acid levels from 8 to 8.9 mg/ dL, 62.0% ( 95% CI, 53.0- 66.4) for uric acid levels from 9 to 9.9 mg/ dL, and 70.7% for uric acid levels of 10 mg/ dL or greater. The increasing trends persisted in subgroups stratified by sex, age group, alcohol intake, body mass index, hypertension, and diabetes. For example, among individuals with normal body mass index ( < 25 kg/ m(2)), the prevalence increased from 5.9% ( 95% CI, 4.8- 7.0), for a uric acid level of less than 6 mg/ dL, to 59.0%, ( 95% CI, 20.1- 97.9) for a uric acid level of 10 mg/ dL or greater. With the original NCEP/ ATP criteria, the corresponding prevalences were slightly lower. CONCLUSIONS: These findings from a nationally representative sample of US adults indicate that the prevalence of the metabolic syndrome increases substantially with increasing levels of serum uric acid. Physicians should recognize the metabolic syndrome as a frequent comorbidity of hyperuricemia and treat it to prevent serious complications. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:442 / 447
页数:6
相关论文
共 42 条
[1]  
Grundy Scott M, 2005, Crit Pathw Cardiol, V4, P198
[2]  
[Anonymous], 2001, GUID DOC US IN VITR
[3]  
[Anonymous], 1996, 3 NAT HLTH NUTR EX S
[4]   The potential role of adenosine in the pathophysiology of the insulin resistance syndrome [J].
Bakker, SJL ;
Gans, ROB ;
ter Maaten, JC ;
Teerlink, T ;
Westerhoff, HV ;
Heine, RJ .
ATHEROSCLEROSIS, 2001, 155 (02) :283-290
[5]   Effects of intravenous adenosine on renal function in healthy human subjects [J].
Balakrishnan, VS ;
Coles, GA ;
Williams, JD .
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 1996, 271 (02) :F374-F381
[6]   A POTENTIAL ROLE FOR ENDOGENOUS ADENOSINE IN CONTROL OF HUMAN GLOMERULAR AND TUBULAR FUNCTION [J].
BALAKRISHNAN, VS ;
COLES, GA ;
WILLIAMS, JD .
AMERICAN JOURNAL OF PHYSIOLOGY, 1993, 265 (04) :F504-F510
[7]   Leptin might be a regulator of serum uric acid concentrations in humans [J].
Bedir, A ;
Topbas, M ;
Tanyeri, F ;
Alvur, M ;
Arik, N .
JAPANESE HEART JOURNAL, 2003, 44 (04) :527-536
[8]   Glucocorticoid use and serum lipid levels in US adults: The Third National Health and Nutrition Examination Survey [J].
Choi, HK ;
Seeger, JD .
ARTHRITIS & RHEUMATISM-ARTHRITIS CARE & RESEARCH, 2005, 53 (04) :528-535
[9]   Alcohol intake and risk of incident gout in men: a prospective study [J].
Choi, HK ;
Atkinson, K ;
Karlson, EW ;
Willett, W ;
Curhan, G .
LANCET, 2004, 363 (9417) :1277-1281
[10]   Pathogenesis of gout [J].
Choi, HK ;
Mount, DB ;
Reginato, AM .
ANNALS OF INTERNAL MEDICINE, 2005, 143 (07) :499-516