ESPE Abstracts (2015) 84 P-1-76

Endothelial Progenitor Cells in Obese Non-Diabetic Children and Adolescents: Relations to Some Metabolic Parameters, Echocardiographic Parameters and Tissue Doppler Imaging

Alaa Ahmeda, Omneya Youssefa & Botheina Thabetb


aAin Shams University, Paediatrics Hospital, Cairo, Egypt; bClinical Pathology Department, Ain Shams University, Cairo, Egypt


Background: Endothelial progenitor cells (EPCs) are involved in the regeneration of the endothelial lining following blood vessel injury. The reduction in the number of EPCs was postulated to be associated with the initiation and progression of cardiovascular disease.

Objective and hypotheses: This study aimed at exploration of the number of EPCs in obese non-diabetic children and adolescents and their relation to the fasting lipid levels, fasting glucose, fasting insulin, homeostasis model assessment for insulin resistance (HOMA-IR), carotid intima media thickness (CIMT), echocardiography as well as parameters of cardiac dysfunction on tissue doppler imaging.

Method: 56 children and adolescents (5–14 years) were chosen randomly from patients seeking medical advice for obesity management at the Obesity Clinic of the Paediatrics Hospital, Ain Shams University. Another group of 32 age and sex matched children and adolescents served as a control group. All underwent anthropometric evaluation, measurement of fasting lipids, glucose, insulin, HOMA-IR, CIMT, echocardiography and tissue doppler imaging. EPCs are the cells expressing CD34 CD144. EPCs were calculated as a percentage of the mononuclear cells.

Results: EPCs were significantly lower in patients compared to controls (P=0.00) and CIMT was significantly higher in patients (P=0.00). Despite showing non-significant correlations with the fasting lipid parameters, fasting insulin, fasting glucose and HOMA yet tissue doppler imaging across the mitral valve showed a significant positive correlation with the EPCs (r=0.283, P=0.034).

Conclusion: Obese non-diabetic children and adolescents have impaired endothelial regeneration and diastolic dysfunction independent of dyslipidaemia or hyperinsulinaemia.

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