Anel Gómez García1, Guillermina García Núñez2, Martha Eva Viveros Sandoval3, Sergio Gutierrez Castellanos4, Cleto Alvarez Aguilar4. 1. Biomedical Research Center of Michoacán, Mexican Institute of Social Security, Morelia, Michoacán, México. anel_gomez04@yahoo.com.mx anel.gomez@imss.gob.mx. 2. Department of Pediatrics, Mexican Institute of Social Security, Morelia, Michoacán, Mexico. 3. Postgrade of Medicine Faculty "Dr Ignacio Chávez" Universidad Michoacana de San Nicolás de Hidalgo, Morelia, Michoacán, Mexico. 4. Regional General Hospital N∘1, Mexican Institute of Social Security, Morelia, Michoacán, Mexico.
Abstract
OBJECTIVE: To investigate the factors associated with platelet activation in obese children. DESIGN: Cross-sectional study. SETTING: Department of Pediatrics of Regional Hospital N∘ 1 of Mexican Institute of Social Security in Morelia, Michoacán, Mexico. PARTICIPANTS: 79 obese and 64 non-obese children between the ages of 5 and 10 years. MAIN OUTCOMES MEASURES: Obese children (body mass index [BMI] >85 in growth curves for Centers for Disease Control/National Center for Health Statistics), and the control group of 64 non-obese children (percentile <85), % body fat, platelet activation was assessed by sP-selectin. Other measures were leptin, uric acid (UA), von Willebrand Factor (vWF), plasminogen activator inhibitor (PAI-1), lipid profile, and glucose. RESULTS: Obese children displayed higher plasma sP-selectin, leptin, PAI-1, and vWF than non-obese children. In the univariate logistic regression analysis, leptin, vWF, UA, and high density lipoprotein (HDL), but not with PAI-1, were factors associated with platelet activation. By stepwise linear regression analysis adjusted by sex and age, the best predictor variables for platelet activation were leptin (β:0.381; t:4.665; P=0.0001), vWF (β:0.211; t:2.926; P=0.004), UA (β:0.166; t:2.146; P=0.034), and HDL (β:-0.215; t:-2.819; P=0.006). CONCLUSIONS: Obese children have a higher risk of developing early platelet activation. Factors associated with platelet activation were Leptin, vWF, UA, and HDL. Further studies involving larger numbers of patients over a longer duration are needed to understand the possible molecular mechanism underlying the association between leptin, vWF, and UA and endothelial activation and/or endothelial damage/dysfunction in obese children and its influence in cardiovascular disease in adults.
OBJECTIVE: To investigate the factors associated with platelet activation in obesechildren. DESIGN: Cross-sectional study. SETTING: Department of Pediatrics of Regional Hospital N∘ 1 of Mexican Institute of Social Security in Morelia, Michoacán, Mexico. PARTICIPANTS: 79 obese and 64 non-obesechildren between the ages of 5 and 10 years. MAIN OUTCOMES MEASURES: Obesechildren (body mass index [BMI] >85 in growth curves for Centers for Disease Control/National Center for Health Statistics), and the control group of 64 non-obesechildren (percentile <85), % body fat, platelet activation was assessed by sP-selectin. Other measures were leptin, uric acid (UA), von Willebrand Factor (vWF), plasminogen activator inhibitor (PAI-1), lipid profile, and glucose. RESULTS:Obesechildren displayed higher plasma sP-selectin, leptin, PAI-1, and vWF than non-obesechildren. In the univariate logistic regression analysis, leptin, vWF, UA, and high density lipoprotein (HDL), but not with PAI-1, were factors associated with platelet activation. By stepwise linear regression analysis adjusted by sex and age, the best predictor variables for platelet activation were leptin (β:0.381; t:4.665; P=0.0001), vWF (β:0.211; t:2.926; P=0.004), UA (β:0.166; t:2.146; P=0.034), and HDL (β:-0.215; t:-2.819; P=0.006). CONCLUSIONS:Obesechildren have a higher risk of developing early platelet activation. Factors associated with platelet activation were Leptin, vWF, UA, and HDL. Further studies involving larger numbers of patients over a longer duration are needed to understand the possible molecular mechanism underlying the association between leptin, vWF, and UA and endothelial activation and/or endothelial damage/dysfunction in obesechildren and its influence in cardiovascular disease in adults.
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