Relationship between insulin resistance, metabolic syndrome components and serum uric acid

被引:54
作者
Adnan, Endy [1 ]
Rahman, Ilham Akbar [2 ]
Faridin, H. P. [1 ]
机构
[1] Hasanuddin Univ, Dept Internal Med, Rheumatol Div, Makassar, South Sulawesi, Indonesia
[2] Hasanuddin Univ, Fac Med, Makassar, South Sulawesi, Indonesia
关键词
Serum uric acid; Metabolic syndrome; Insulin resistance; CARDIOVASCULAR RISK; BLOOD-PRESSURE; HYPERURICEMIA; ASSOCIATION; PREDICTS;
D O I
10.1016/j.dsx.2019.04.001
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Metabolic syndrome is cluster of abnormality related with increasing cardiovascular events. Hyperuricemia is level of uric acid more than 7 mg/dL for men. Some research have reported relation between metabolic syndrome mediated by insulin resistance with increasing of serum uric acid level. Objective: Assess relationship between insulin resistance and metabolic syndrome components with the level of serum uric acid. Method: Observational study with cross sectional approach conducted on 102 outpatient subjects at Dr. RSUP Wahidin Sudirohusodo (RSWS) hospital and Hasanuddin University Hospital in the period of July -September 2018. Results: Subjects with IR were found to be significantly higher for having MetS (88.23% vs. 11.77% p = 0,000). In subjects with IR, the average serum uric acid level was higher compared to non-IR subjects, but this difference was not significant (6.63 vs 6.42mg/dL; P = 0.325). In subjects with MetS, the average serum uric acid level was higher compared to subjects with non-MetS but this difference was not significant (6.62 vs. 6.28 mg/dL; P = 0.556). No significant relationship was found between IR and MetS with serum uric acid level. Conclusion: Insulin resistance is related to the incidence of MetS and in both of these circumstances an independent tendency is found to increase uric acid levels. The role of insulin resistance in the relationship between metabolic syndrome and uric acid levels was not proven in this study. (C) 2019 Diabetes India. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:2158 / 2162
页数:5
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