Details

Autor(en) / Beteiligte

• Zdanowicz, Katarzyna
• Białokoz-Kalinowska, Irena
• Lebensztejn, Dariusz M

Titel

Non-alcoholic fatty liver disease in non-obese children

Ist Teil von

• Hong Kong Medical Journal, 2020-10, Vol.26 (5), p.459-462

Ort / Verlag

Hong Kong: Hong Kong Academy of Medicine

Erscheinungsjahr

2020

Quelle

EZB Electronic Journals Library

Beschreibungen/Notizen

• Introduction Non-alcoholic fatty liver disease (NAFLD) is a broad spectrum of liver diseases, morphologically characterised by fat accumulation in [greater than]5% of hepatocyte in the absence of other cause of steatosis.1 Less-common factors of hepatic steatosis include metabolic disorders (eg, cystic fibrosis, Wilson's disease, alpha-1 antitrypsin deficiency, galactosaemia, hereditary fructose intolerance), general or systemic disorders (eg, celiac disease, hepatitis C, obstructive sleep apnoea, type 1 diabetes), starvation, malnutrition, total parenteral nutrition, and drug toxicity.2 In recent decades, the increase in the prevalence of NAFLD is related to the global obesity epidemic and is considered to be a hepatic manifestation of the metabolic syndrome.2 Exposure to certain factors such as maternal overnutrition, gestational diabetes mellitus, Caesarean section, intrauterine growth retardation, and antibiotic use during pregnancy and infancy may be associated with an increased risk of NAFLD in children. Metabolically obese, lean NAFLD patients are non-obese subjects (BMI [lesser than]95th percentile of age, overweight is not an exclusion criterion) with or without coexisting increased waist circumference and visceral adipose tissue.2 Epidemiology The incidence of lean NAFLD in adolescents varies widely, ranging from 8% in the US4 to 16% in the Asia-Pacific region.4 5 Large discrepancies in the occurrence rates may be related to different inclusion criteria and cut-off points for non-obese NAFLD.6 7The prevalence of lean NAFLD differs significantly due to urbanisation and wealth of different regions of the world, as well as the associated diet and physical activity levels.8 Visceral adiposity According to Javed et al,9 BMI may be wrongly classified in over a quarter of children with excess adiposity. Compared with other anthropometric measurements such as waist circumference, waist-to-hip ratio, and BMI, SAD showed stronger correlations with metabolic syndrome risk factors.12 Genetic and environmental factors Genetic factors associated with increased risk of developing NAFLD in non-obese patients include nucleotide polymorphisms in patatin-like phospholipase domain-containing 3 (PNPLA3) [rs738409], cholesteryl ester transfer protein (CETP) [rs12447924 and rs12597002], transmembrane 6 superfamily member 2 (TM6SF2), and apolipoprotein 3 (APCO3) [rs2854116 and rs2854117].2 13 The microsomal triglyceride transfer protein (MTP), membrane-bound O-acyltransferase domain-containing protein 7 (MBOAT7), peroxisome proliferator-activated receptor-γ coactivator (PPARGC1A), heme oxygenase-1 (HO-1), and hypoxia inducible factor 3 alpha subunit (HIF3A) genes represent NAFLD risk factors in the paediatric population, but to date studies have only involved obese children.13 The relationship between dietary fructose intake and NAFLD has also been described. [...]levels of alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase, low-density lipoprotein, high-density lipoprotein, and uric acid did not differ between groups.16 Non-obese NAFLD subjects, deprived of other metabolic risk factors, more frequently had insulin resistance.17 In the US, insulin resistance was found to be more common in lean adolescents with NAFLD than in lean healthy controls, although this difference was not statistically significant.4 Histological features Liver biopsy is the gold standard in diagnosing and grading the severity of NAFLD.1 There have been limited studies devoted to the evaluation of histological features in lean children with NAFLD.