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Serum uric acid level may be a predictor of metabolic syndrome in adolescents, a new study reports. The findings offer clinicians another diagnostic tool for identifying children who are at a higher risk for developing cardiovascular disease and type 2 diabetes mellitus.
To examine the relationship between serum UA and metabolic syndrome, researchers divided 613 boys aged 10 to 15 years into 4 groups according to their UA levels, with UA-1 being the lowest and UA-4 the highest, and followed them for a mean of 2.7 years.
At the end of follow-up, 19 (3.1%) boys had developed metabolic syndrome. Significant links were found between baseline UA level and waist circumference, systolic blood pressure, high-density lipoprotein cholesterol (HDL-C), and triglycerides.
Boys in the UA-4 group were markedly more likely to have abnormal waist circumference, blood pressure, and HDL-C and had a 6.39 greater likelihood of developing metabolic syndrome than boys in the UA-1 group. Serum UA level greater than 7.6 mg/dL was an independent predictor of metabolic syndrome, as were high waist circumference and blood pressure.
Obesity may be the most important contributor to metabolic syndrome in adolescents with high UA levels, the researchers say. The UA-4 group had a 14-fold greater likelihood of becoming obese than the UA-1 group-about 4 times higher than the probability for the other components of metabolic syndrome.
Unlike most studies in adults, this one found no significant association between high UA levels and fasting plasma glucose. The researchers speculate that increased insulin secretion is able to compensate for insulin resistance until middle age. They note that a lack of data on plasma insulin concentrations limited their results.
The International Diabetes Federation has defined the components of metabolic syndrome in children and adolescents and cautions that these risk factors continue into adulthood. Elevated UA is considered a nontraditional component that may raise the risk of cardiovascular disease and type 2 diabetes mellitus independently by increasing circulating oxygen radicals and promoting oxidation of lipids, resulting in vascular endothelial dysfunction, inflammation, impaired nitric oxide production, atherosclerosis, and clot formation.
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