Assessment of cardiometabolic risk factor clustering in obese children and adolescents with metabolic syndrome

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Assessment of cardiometabolic risk factor clustering in obese children and adolescents with metabolic syndrome

https://karger.com/hrp/article/94/Suppl.%201/1/823910/Abstracts

Hormone Research in Paediatrics
Volume 94, Issue Suppl. 1
Issue release date: September 2021
European Society for Paediatric Endocrinology (ESPE)
59th Annual Meeting, Online, September 2021: Abstracts

ePoster Category 2 Fat, metabolism and obesity

P2-205 / Assessment of cardiometabolic risk factor clustering in obese children and adolescents with metabolic syndrome

Athanasia Tragomalou1,2, Maria Manou1,2, Sofia Loukopoulou3, Maria Binou1, Marina Papadopoulou1, Penio Kassari1,2, Evangelia Charmandari1,2

  1. Outpatient Clinic For the Prevention and Management of Overweight and Obesity, Division of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, ‘Aghia Sophia’ Children’s Hospital, Athens, Greece;
  2. Division of Endocrinology and Metabolism, Center of Clinical, Experimental Surgery and Translational Research, Biomedical Research Foundation of the Academy of Athens, Athens, Greece;
  3. Department of Pediatric Cardiology, ‘Aghia Sophia’ Children’s Hospital, Athens, Greece

Background: Obesity in childhood and adolescence has reached epidemic proportions. Endothelial dysfunction, as a consequence of dyslipidemia, hypertension, insulin resistance and inflammation, imposes a substantial risk for the development of metabolic syndrome (MS) in childhood and compromises the health of the pediatric population by promoting premature development of atherosclerotic cardiovascular disease.

Aim: To investigate the cardiovascular risk in obese children and adolescents with MS compared with their obese counterparts without MS.

Patients and Methods: Eighty eight (n = 88) obese children and adolescents [mean age ± SD: 13.1 ± 1.9 years; 53 males (60.2%) and 35 females (39.8%); 14 prepubertal (15.9%) and 74 pubertal (84.1%)] with MS and sixty (n = 60) obese children and adolescents without MS [12.2 ± 2.1 years; 37 males (61.7%) and 23 females (38.3%); 18 prepubertal (30%) and 42 pubertal (70%)] were studied prospectively for one year. All participants received personalized advice on diet and exercise, while 26 (29.5%) participants in the MS group and 13 (21.7%) participants in the control group also received metformin. Biochemical and endocrinologic investigations, oral glucose tolerance test, echocardiography, ultrasonography of the carotid arteries and liver were performed at the beginning and at the end of study.

Results: Systolic and diastolic blood pressure was significantly higher in children with MS (127.9±13.1 and 76.7±11.3mmHg, respectively) than those without MS (116.6±10.5 and 68.2±9.2mmHg, P < 0.001). At the beginning of the study (t0), subjects with MS had significantly lower HDL [39.1±1.2 vs. 45.2±1.2 mg/dl, P < 0.001], and higher triglycerides (125.1±1.6 vs. 86.5±1.5 mg/dl, P < 0.001) and insulin (30.4±1.6 vs. 20.7±1.4 μIU/ml, P < 0.001] concentrations compared with the control group. The carotid intima-media thickness (cIMT) at t0 was 0.8±1.1mm in the MS group and 0.7±1.1mm in the non MS group, respectively (normal range: 0.49±0.03mm), whereas after 1 year of intervention cIMTt12improved significantly only in children with MS (0.5±0.2mm, P < 0.05). Furthermore, patients with MS and ≥ 3 risk factors had significantly higher cIMT compared to those with 2 or less risk factors. Interventricular septal end diastole and systole were significantly higher in patients with MS (8.4±1.7 mm and 9.0±1.3 mm, respectively) than the control group (7.8±1.2 mm and 8.2±1.3 mm, P < 0.05). Hepatic steatosis was identified in 69 (78%) of the participants with MS and in 34 (56.7%) obese without MS.

Conclusions: Our findings demonstrate increased cardiovascular risk in children and adolescents with MS, as well as an improvement in certain cardiovascular parameters following intervention.

Conference Proceedings / Horm Res Paediatr 2021;94(suppl 1):1–445 DOI: 10.1159/000518849