Non-Alcoholic Fatty Liver Disease and the Left Ventricle Mass Index in Obese Children
|Beray Selver1, Enver Simsek2*, Ugur Kocabas3 and Yildiz Dallar1|
|1Department of Pediatrics, Ankara Research and Training Hospital, Ankara, Turkey|
|2Department of Pediatrics, Division of Endocrinology, Eskisehir Osmangazi University, School of Medicine, Eskisehir, Turkey|
|3Department of Cardiology, Ankara Research and Training Hospital, Ankara, Turkey|
|Corresponding Author :||Prof. Dr. Enver Simsek
Department of Pediatrics
Division of Pediatric Endocrinology
Eskisehir Osmangazi University
School of Medicine, Eskisehir, Turkey
E-mail: [email protected]
|Received February 24, 2012; Accepted May 26, 2012; Published May 25, 2012|
|Citation: Selver B, Simsek E, Kocabas U, Dallar Y (2012) Non-Alcoholic Fatty Liver Disease and the Left Ventricle Mass Index in Obese Children. J Metabolic Synd 1:110. doi:10.4172/2167-0943.1000110|
|Copyright: © 2012 Selver B. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.|
Objective: To investigate Nonalcoholic Fatty Liver Disease (NAFLD), the Left Ventricle Mass Index (LVMI), and the relationship between NAFLD and LVMI in obese children.
Material and methods: Systolic (SBP) and Diastolic (DBP) Blood Pressure and waist and hip circumferences were measured. Fasting blood glucose and insulin concentrations, total cholesterol, and Triglycerides (TG) were assayed. The diagnosis of NAFLD was based on sonographic evidence of a fatty liver. The Left Ventricle Mass (LVM) was calculated from two-dimensionally guided M-mode echocardiographic measurements of the left ventricle. LVMI was calculated as LVM (g)/height (m)2.7 and Left Ventricular Hypertrophy (LVH) was defined as LVMI ≥ 95th percentile for age and gender
Results: Forty-three obese children with NAFLD, 55 obese children without NAFLD, and 48 non-obese controls were studied. Fasting insulin, homeostasis model assessment-estimated insulin resistance (HOMA-IR) index, TG, and total cholesterol levels in the obese children were significantly higher than in the controls (all p < 0.001); SBP and DBP in the obese children were also higher than in the controls. LVMI was higher in the obese children (p < 0.001), although the mean LVMI did not differ significantly between obese children with and without NAFLD (p > 0.05). The prevalence of LVH differed significantly between the obese groups and controls (all p < 0.001), while there was no significant difference between the obese subjects with and without NAFLD. LVH was present in 5 of 48 (10.4%) control subjects, 25 of 79 (31.6%) obese subjects with normotensive subjects, and 6 of 19 (36.8%) obese subjects with hypertension. The prevalence of LVH differed significantly between the obese groups and controls (all p < 0.001), whereas no significant difference was observed between obese subjects with or without hypertension (p > 0.05). In a multiple linear regression analysis, NAFLD, SBP, and DBP were not correlated with LVMI. The LVMI was closely related to the Body Mass Index-Standard Deviation Score (BMI-SDS), and Liver Longitudinal Dimension (LLD) percentile. The BMI-SDS was the only independent predictor of NAFLD and LVMI.
Conclusions: LVH and NAFLD are two important and independent covariates in obese children. Obese children with or without hypertension have significant LVH as compared with non-obese control subjects. NAFLD and casual blood pressure measurements are not predictors of LVMI in obese children.