Non-Alcoholic Fatty Liver Disease (NAFLD) in Overweight and Obese Children and Adolescents

Research Article

Austin J Obes & Metab Synd. 2020; 4(2): 1017.

Non-Alcoholic Fatty Liver Disease (NAFLD) in Overweight and Obese Children and Adolescents

Schiel R1*, Heinrichs M1, Stein G2, Bambauer R3 and Steveling A4

1Department of Diabetes and Metabolic Diseases, MEDIGREIF-Inselklinik Heringsdorf GmbH, Ostseebad Heringsdorf, Germany

2Friedrich-Schiller-University, Internal Medicine, Jena, Germany

3Formerly Institute for Blood Purification, Homburg, Germany

4University of Greifswald, Internal Medicine A, Greifswald, Germany

*Corresponding author: Ralf Schiel, MEDIGREIFInselklinik Heringsdorf GmbH, Setheweg 11, D-17424 Ostseebad Heringsdorf, Germany

Received: June 03, 2020; Accepted: July 01, 2020; Published: July 08, 2020


Over the last decades overweight, obesity and Non-Alcoholic Fatty Liver Disease (NAFLD) in childhood and adolescence increased. NAFLD is strongly associated with insulin resistance, hypertension, dyslipidemia and other proatherogenic conditions. It was the aim of the trial to analyze the prevalence of NAFLD, risk factors and comorbidities in a cohort of overweight and obese children and adolescents.

Patients and Methods: Totally 79 children and adolescents with overweight/ obesity (age 13.3 ± 2.4 years, BMI 33.4 ± 6.5 kg/m², BMI-SDS 2.72 ± 0.52) participated in a Structured Treatment and Teaching Program [STTP] (36.1 ± 5.9 days) for weight reduction were included.

Results: NAFLD was diagnosed in 42/79 (53%) of patients. Patients with NAFLD were older (14.0±2.2 vs 12.5±2.5 years, p=0.005), had a higher BMI (36.8±6.4 vs 29.6±4.1 kg/m2, p<0.001), BMI-SDS (2.96±0.48 vs 2.45±0.42, p<0.001) and higher fasting C-peptide (0.77±0.33 vs 0.61±0.28 nmol/l, p=0.018), fasting insulin concentrations (23.4±11.4 vs 15.4±12.1 μIU/ml, p=0.004) and HOMA-index (4.80±2.48 vs 3.22±3.46, p=0.022). Moreover patients with NAFLD had higher values in thickness of A. carotis intima. After an in-patient treatment lasting in the mean 5 weeks children/adolescents reached a mean weight reduction of 3.8±2.7 (range, -15.5-+0.8) kg (p<0.001) along with an improvement of risk parameters. The most important factors associated with NAFLD (R-square=0.444) revealed by the multivariate analysis were: body weight (ß=0.407, p<0.001), HOMA (ß=0.265, p=0.014) and HDL-cholesterol (ß=-0.229, p=0.018) at onset of the trial.

Discussion: Children/adolescents with NAFLD were more likely overweight or obese, had more frequently metabolic risk factors and a higher thickness of A. carotis intima media. The data also suggest an improvement in metabolic and cardiovascular risk factors after a significant weight reduction.

Keywords: Body Mass-Index (BMI); C-peptide; HOMA-index; Cardiovascular Disease; Diabetes Mellitus


Over the last two decades Non-Alcoholic Fatty Liver Disease (NAFLD) in childhood and adolescence gained more and more interest. Already in 2006 Patton et al. concluded “Although population prevalence is very difficult to establish, Nonalcoholic Fatty Liver Disease (NAFLD) is probably the most common cause of liver disease in the preadolescent and adolescent age group “[1]. A recently published meta-analysis suggested a prevalence ratio for NAFLD in children/adolescents aged 5 to 18 years with obesity relative to those of a “healthy weight” of 26.1 (95% Confidence Interval [CI], 9.4-72.3) [2]. Anderson et al. found a “pooled mean prevalence of NAFLD in children from general population studies” of 7.6% (95% CI: 5.5- 10.3%) and of 34.2% (95% CI 27.8-41.2%) in studies based on child obesity clinics” [3].

Important reasons for the great variability in awareness and prevalence rates of NAFLD are uncertainities in respect of diagnosis and a lack of simple, non-invasive diagnostic tests [4]. According to Bellentani and Marino in NAFLD there is an accumulation of fat in the liver without excessive alcohol consumption or other known liver pathologies [5]. Mostly NAFLD is defined by the ultrasonographic appearance of the liver (mild to severe steatosis) [4,6,7]. But, also biomarkers can play an important role: In some studies Alanine (ALT) and aspartate Aminotransferfase (AST) where used [3,8], although Anderson et al. concluded that “currently” there is “no consensus on the thresholds of liver enzymes that should be used to indicate NAFLD” [3]. Up to day according to Shah et al. [9], Shakir et al. [10], Vos et al. [11] and Chalasani et al. [12] liver biopsy is the gold-standard approach to determine the presence and severity of NAFLD.

A variety of analyses have shown, that additional to overweight and obesity NAFLD is strongly associated with insulin resistance, hypertension, dyslipidemia and other pro-atherogenic conditions (like inflammatory disorders or endothelial dysfunction) [3,4,13,14]. Pacificio et al. [13] wrote in 2011: “Pathological studies have shown that atherosclerosis is an early process beginning in childhood […]. There is a positive correlation between the extent of early atherosclerotic lesions in the […] carotid arteries and cardiovascular risk factors […]”. The “Guide for General Practitioners” [10] concluded: “Successful management of pediatric NAFLD requires that clinicians identify children with the highest risk through early screening, understand the comorbidities, and offer a multidisciplinary treatment approach that emphasizes diet and physical activity modification […].” On this background it was the aim of the present trial to analyze the prevalence of NAFLD, risk factors and comorbidities in a cohort of overweight and obese children and adolescents admitted to a specialized hospital.

Patients and Methods

Totally 79 children and adolescents with overweight and obesity successively admitted to our hospital were included in the trial (inclusion criteria: BMI [Body Mass Index]/BMI-SDS [Body Mass Index Standard Deviation Score] > 97. Percentile [15] and/or diagnosis for admittance: code according to ICD-10- GM-2019 “E66.0”, html). The patients participated in a Structured Treatment and Teaching Program [STTP] for weight reduction [15,16]. The STTP was evaluated and demonstrated a good long-term effect (weight reduction and stabilization) over a period of 12 months [17,18]. Further details of the study protocol used in the present trial were published in 2019 [19].

Schedule of the trial

At the beginning of the trial and at the end of the inpatient treatment period (36.1±5.9 [22-57] days) the following examinations were performed:

• In all patients physical examinations were performed.

• Measurements of height and weight were assessed with patients wearing light clothing and without shoes. BMI and BMI-SDS were calculated according to the formulae “BMI=kg/m2” and “BMISDS=([ BMI/M(t)]L(t)-1)/(L(t)*S(t)” (M(t), L(t) and S(t) are pre-defined parameters depending on age(t) and sex [15].

• Body composition analyses were done using a Body composition analyzer (BC418MA, TANITA Europe GmbH, Sindelfingen, Germany).

• Blood pressure in the sitting position was measured after the patients had rested for 10 min by using a standard sphygmomanometer according to the World Health Organization (WHO) recommendations [20]. In all patients a 24-hour-monitoring was performed (Premo Trend, Zimmer Elektromedizin, Neu-Ulm, Germany).

• Ultrasound examination (Siemens Acuson X300PE, München, Germany): On ultrasound images the diagnosis steatosis hepatis (fatty liver) was given, if the liver looks brighter than normal (but not lumpy or shrunken like cirrhotic livers). NAFLD was diagnosed according to ultrasonographic appearance of fatty liver [4] without anamnesis of alcohol consumption or other known liver pathologies [5].

• Measurements of carotid Intima-Media Thickness (IMT) were done by one physician performing 5 measurements on each side and calculating the mean. Definition of normal values was according to the German standard [21].

• Blood-glucose (glucose-oxidase-method, Speedy, Müller Gerätebau GmbH, Saalfeld, Germany) and HbA1c-measurements (DCA2000®-method, Bayer Diagnostics, Leverkusen, Germany, following DCCT-standard [HbA1c/mean normal] x mean according to the DCCT-standard [22]) were done directly in the laboratory of the Medigreif Inselklinik Heringsdorf GmbH using blood samples derived from finger pricking. Additionally venous blood samples taken in the morning of the first day after hospital admission (at onset/beginning of the trial) and at the last day of patients’ in-hospital stay (at the end of the trial) following an overnight fasting period were analyzed (Laborgemeinschaft IMD, Prof. Dr. med. G. Menzel, Pappelallee 1, 17489 Greifswald, Germany) from all patients. The parameters analyzed and the methods of measurement are shown in Table 1.