Shima Dowla1, Stella Aslibekyan2, Amy Goss3, Kevin Fontaine4, Ambika P Ashraf5. 1. Department of Health Behavior, University of Alabama at Birmingham, Birmingham, AL, USA; School of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA. 2. Department of Epidemiology, University of Alabama at Birmingham, Birmingham, AL, USA. 3. Department of Nutrition, University of Alabama at Birmingham, Birmingham, AL, USA. 4. Department of Health Behavior, University of Alabama at Birmingham, Birmingham, AL, USA. 5. Division of Pediatric Endocrinology, Department of Pediatrics, University of Alabama at Birmingham, Birmingham, AL, USA. Electronic address: AAshraf@peds.uab.edu.
Abstract
BACKGROUND: With the increasing prevalence of childhood obesity, nonalcoholic fatty liver disease (NAFLD) has emerged as the most common cause of pediatric chronic liver disorder. Factors underlying the pathophysiology of NAFLD remain poorly defined. OBJECTIVE: This study aimed to describe the metabolic characteristics of children with NAFLD differing in race/ethnicity and to test associations between dyslipidemia and NAFLD. METHODS: A retrospective chart review was conducted at a tertiary referral university hospital among 309 children with a diagnosis of NAFLD. RESULTS: Participants (mean age 12.5 ± 3.4 years) were 64% male, 63% white, 23% Hispanic, and 14% black. Hispanic children were diagnosed with NAFLD at a significantly younger age (10.6 ± 3.1 years, P < .0001) and lower body mass index (31.5 ± 6.8 kg/m2, P < .0001) than their white and black counterparts. For the entire cohort, prevalence of systolic hypertension was 41%, diabetes 14%, elevated cholesterol 42%, elevated non-high-density lipoprotein cholesterol (non-HDL-C) 58%, elevated low-density lipoprotein cholesterol 36%, elevated triglycerides (TG) 88%, and low high-density lipoprotein cholesterol 77%. Whites had elevated non-HDL-C, low-density lipoprotein cholesterol, and TG compared to blacks or Hispanics. Serum TG and non-HDL-C were significantly correlated to alanine aminotransferase (r = 0.18, P = .01; r = 0.16, P = .02), respectively, and persisted after adjusting for age and body mass index. CONCLUSION: Cardiometabolic derangements, especially dyslipidemia, are highly prevalent in children with NAFLD and differ based on race/ethnicity. Serum TG and non-HDL-C may play an important role in the pathophysiology of pediatric NAFLD.
BACKGROUND: With the increasing prevalence of childhood obesity, nonalcoholic fatty liver disease (NAFLD) has emerged as the most common cause of pediatric chronic liver disorder. Factors underlying the pathophysiology of NAFLD remain poorly defined. OBJECTIVE: This study aimed to describe the metabolic characteristics of children with NAFLD differing in race/ethnicity and to test associations between dyslipidemia and NAFLD. METHODS: A retrospective chart review was conducted at a tertiary referral university hospital among 309 children with a diagnosis of NAFLD. RESULTS: Participants (mean age 12.5 ± 3.4 years) were 64% male, 63% white, 23% Hispanic, and 14% black. Hispanic children were diagnosed with NAFLD at a significantly younger age (10.6 ± 3.1 years, P < .0001) and lower body mass index (31.5 ± 6.8 kg/m2, P < .0001) than their white and black counterparts. For the entire cohort, prevalence of systolic hypertension was 41%, diabetes 14%, elevated cholesterol 42%, elevated non-high-density lipoprotein cholesterol (non-HDL-C) 58%, elevated low-density lipoprotein cholesterol 36%, elevated triglycerides (TG) 88%, and low high-density lipoprotein cholesterol 77%. Whites had elevated non-HDL-C, low-density lipoprotein cholesterol, and TG compared to blacks or Hispanics. Serum TG and non-HDL-C were significantly correlated to alanine aminotransferase (r = 0.18, P = .01; r = 0.16, P = .02), respectively, and persisted after adjusting for age and body mass index. CONCLUSION: Cardiometabolic derangements, especially dyslipidemia, are highly prevalent in children with NAFLD and differ based on race/ethnicity. Serum TG and non-HDL-C may play an important role in the pathophysiology of pediatric NAFLD.
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