Abstract
Background: To establish the rate of agreement in predicting metabolic syndrome (MS) in different pediatric classifications using percentiles or fixed cut-offs, as well as exploring the influence of cholesterol. Subjects and methods: Cross-sectional study in a tertiary care center. Nine hundred and twenty-three obese children and adolescents were evaluated for metabolic characteristics, cholesterol levels, the agreement rate and prevalence of MS across age subgroups with pediatric National Cholesterol Education Program/Adult Treatment Panel III (NCEP-ATP III) and International Diabetes Federation (IDF) classifications. Results: The overall prevalence of MS was 36.2% and 56.7% with NCEP-ATP III and IDF. The overall concordance was fair (k: 0.269), with substantial values observed only in children older than 10 (k: 0.708) and 16 yr (0.694). Concordant subjects for both classifications, ≤6 yr, had higher triglycerides, blood pressure (p<0.05) and lower HDL-cholesterol (p<0.0001), with respect to those found to be discordant. Concordant subjects ranging 6–10 yr had all parameters higher than those discordant for IDF (p<0.01) and insulin resistance (p<0.05) than those discordant for NCEP-ATP III. Concordant subjects ≥10 yr presented more altered parameters than those included only in NCEP-ATP III (p<0.05). Overt glucose alterations were uncommon (7.4%; confidence interval 95% 0.1–14.9%), although glucose was modestly higher in MS subjects (p<0.01). Total and LDL-cholesterol was lower in subjects with MS than in those without (p<0.05), and in concordant rather than discordant subjects (p<0.05). Conclusions: Classifications of MS do not identify the same pediatric population. Subjects who satisfied any classification were the most compromised. Lipid alterations were precocious in the youngest. Obese youths with MS presented lower total and LDL-cholesterol.
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Lobstein T, Frelut ML. Prevalence of overweight among children in Europe. Obes Rev 2003, 4: 195–200.
Sinha R, Fisch G, Teague B, et al. Prevalence of impaired glucose tolerance among children and adolescents with marked obesity. N Engl J Med 2002, 46: 802–10.
Cruz ML, Weigensberg MJ, Huang TT-K, Ball G, Shaibi GQ, Goran MI. The metabolic syndrome in overweight Hispanic youth and the role of insulin sensitivity. J Clin Endocrinol Metab 2004, 89: 108–13.
Cook S, Weitzman M, Auinger P, Nguyen M, Dietz WH. Prevalence of a metabolic syndrome phenotype in adolescents: findings from the Third National Health and Nutrition Examination Survey, 1988–1994. Arch Pediatr Adolesc Med 2003, 57: 821–7.
de Ferranti SD, Gauvreau K, Ludwig DS, Neufeld EJ, Newburger JW, Rifai N. Prevalence of the metabolic syndrome in American adolescents: findings from the Third National Health and Nutrition Examination Survey. Circulation 2004, 110: 2494–7.
Weiss R, Dziura J, Burgert TS, et al. Obesity and the metabolic syndrome in children and adolescents. N Engl J Med 2004, 350: 2362–74.
Zimmet P, Alberti G, Kaufman F, et al. International Diabetes Federation Task Force on Epidemiology and Prevention of Diabetes. The metabolic syndrome in children and adolescents. Lancet 2007, 369: 2059–61.
Caranti DA, Lazzer S, Damaso AR, et al. Prevalence and risk factors of metabolic syndrome in Brazilian and Italian obese adolescents: a comparison study. Int J Clin Pract 2008, 62: 1526–32.
Seo SJ, Lee HY, Lee SW. The prevalence of the metabolic syndrome in Korean children and adolescents: comparisons of the criteria of Cook et al., Cruz and Goran, and Ferranti et al. Yonsei Medical J 2008, 49: 563–72.
Di Bonito P, Forziato C, Sanguigno E, et al. Prevalence of the metabolic syndrome using ATP-derived definitions and its relation to insulin-resistance in a cohort of Italian outpatient children. J Endocrinol Invest 2010, 33: 806–9.
Steinberger J, Daniels SR, Eckel RH, et al. Progress and challenges in metabolic syndrome in children and adolescents: a scientific statement from the American Heart Association Atherosclerosis, Hypertension, and Obesity in the Young Committee of the Council on Cardiovascular Disease in the Young; Council on Cardiovascular Nursing; and Council on Nutrition, Physical Activity, and Metabolism. Circulation 2009, 119: 628–47.
Viner RM, Segal TY, Lichtarowicz-Krynska E, Hindmarsh P. Prevalence of the insulin resistance syndrome in obesity. Arch Dis Child 2005, 90: 10–4.
Sen Y, Kandemir N, Alikasifoglu A, Gonc N, Ozon A. Prevalence and risk factors of metabolic syndrome in obese children and adolescents: the role of the severity of obesity. Eur J Pediatr 2008, 167: 1183–9.
Cacciari E, Milani S, Balsamo A, et al. Italian cross-sectional growth charts for height, weight and BMI (2 to 20 yr). J Endocrinol Invest 2006, 29: 581–93.
Prodam F, Trovato L, Demarchi I, et al. Unacylated, acylated ghrelin and obestatin levels are differently inhibited by oral glucose load in pediatric obesity: association with insulin sensitivity and metabolic alterations. e-SPEN Eur J Clin Nutr Metab 2011, 6: e109–15.
McCarthy HD, Jarrett KV, Crawley HF. The development of waist circumference percentiles in British children aged 5.0 ± 16.9 y. Eur J Clin Nutr 2001, 55: 902–7.
Daniels SR, Greer FR. Lipid screening and cardiovascular health in childhood. Pediatrics 2008, 122: 198.
National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents. The fourth report on the diagnosis, evaluation and treatment of high blood pressure in children and adolescents. Pediatrics 2004, 114: 555–76.
Bokor S, Frelut ML, Vania A, et al. Prevalence of metabolic syndrome in European obese children. Int J Pediatr Obes 2008, 3(Suppl 2): 3–8.
Lafortuna CL, Adorni F, Agosti F, et al. Prevalence of the metabolic syndrome among extremely obese adolescents in Italy and Germany. Diabetes Res Clin Pract 2010, 1: 14–21.
Bustos P, Saez K, Gleisner A, Ulloa N, Calvo C, Asenjo S. Metabolic syndrome in obese adolescents. Pediatr Diabetes 2010, 11: 55–60.
Tzoulaki I, Sovio U, Pillas D, et al. Relation of immediate postnatal growth with obesity and related metabolic risk factors in adulthood: the northern Finland birth cohort 1966 study. Am J Epidemiol 2010, 171: 989–98.
Kashyap S, Belfort R, Gastaldelli A, et al. A sustained increase in plasma free fatty acids impairs insulin secretion in nondiabetic subjects genetically predisposed to develop type 2 diabetes. Diabetes 2003, 52: 2461–74.
Reinehr T, de Sousa G, Toschke AM, Andler W. Comparison of metabolic syndrome prevalence using eight different definitions: a critical approach. Arch Dis Child 2007, 92: 1067–72.
Kleber M, de Sousa G, Papcke S, Reinehr T. Risk factors for impaired glucose tolerance in obese children and adolescents. World J Diabetes 2010, 1: 129–34.
Mayor S. Nearly 23,000 people in England aged under 18 have diabetes, survey shows. BMJ 2010, 340: c980.
Saad R, Gungor N, Arslanian S. Progression from normal glucose tolerance to type 2 diabetes in a young girl: longitudinal changes in insulin sensitivity and secretion assessed by the clamp technique and surrogate estimates. Pediatr Diabetes 2005, 6: 95–9.
Tfayli H, Arslanian S. Pathophysiology of type 2 diabetes mellitus in youth: the evolving chameleon. Arq Bras Endocrinol Metab 2009, 53: 165–74.
Preiss D, Sattar N. Lipids, lipid modifying agents and cardiovascular risk: a review of the evidence. Clin Endocrinol (Oxf) 2009, 70: 815–28.
Simonen P, Gylling H, Howard AN, Miettinen TA. Introducing a new component of the metabolic syndrome: low cholesterol absorption. Am J Clin Nutr 2000, 72: 82–8.
Briand F, Thiéblemont Q, Muzotte E, Sulpice T. High-fat and fructose intake induces insulin resistance, dyslipidemia, and liver steatosis and alters in vivo macrophage-to-feces reverse cholesterol transport in hamsters. J Nutr 2012, 142: 704–9.
Yang ZH, Miyahara H, Takeo J, Katayama M. Diet high in fat and sucrose induces rapid onset of obesity-related metabolic syndrome partly through rapid response of genes involved in lipogenesis, insulin signalling and inflammation in mice. Diabetol Metab Syndr 2012, 4: 32.
Alsaleh A, Frost GS, Griffin BA, et al; RISCK Study investigators. PPARγ2 gene Pro 12Ala and PPARα gene Leu 162Val single nucleotide polymorphisms interact with dietary intake of fat in determination of plasma lipid concentrations. J Nutrigenet Nutrigenomics 2011, 4: 354–66.
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Prodam, F., Ricotti, R., Genoni, G. et al. Comparison of two classifications of metabolic syndrome in the pediatric population and the impact of cholesterol. J Endocrinol Invest 36, 466–473 (2013). https://doi.org/10.3275/8768
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DOI: https://doi.org/10.3275/8768