Pediatric Nonalcoholic Fatty Liver Disease
Abstract and Introduction
Abstract
Purpose of review Nonalcoholic fatty liver disease (NAFLD) is a multicluster disease ranging from intrahepatic simple steatosis to nonalcoholic steatohepatitis (NASH). During the last decade, NAFLD has reached epidemic proportions in overweight/obese children. In this manuscript, we review all recent advances in paediatric NAFLD.
Recent findings Paediatric NAFLD displays some common aspects with the adult form of disease. However, recent findings have demonstrated that regarding development of NAFLD in children, due to the absence of long-time confounding factors, it may be more appropriate to investigate genetic and pathogenetic origins of the disease. Furthermore, as the histological pattern of paediatric NAFLD is different from those observed in adults, specific diagnostic/management programmes and diagnostic scores have been recently developed. Accordingly, several studies demonstrated that both lifestyle intervention and pharmacological treatments should be adequate to the specific pattern of NAFLD in children.
Summary Results of this year's investigations further elucidated the histological features and genetic background that characterize paediatric NAFLD; the closed association of disease development with the cross-talk between different cells and organs; limitations of diagnostic tools borrowed from adult studies and the need of further clinical trial.
Introduction
Nonalcoholic fatty liver disease (NAFLD) comprises a cluster of differentially graded liver diseases ranging from intrahepatic fat accumulation (simple steatosis) to necro-inflammation, hepatocyte ballooning and fibrosis that represent the main features of nonalcoholic steatohepatitis (NASH). During the last decade, paediatric NAFLD has reached epidemic proportions, becoming one of the most frequent chronic liver diseases in the global child population. Epidemiological data obtained by noninvasive and invasive diagnostic tests indicate that NAFLD affects approximately 3–10% of the lean children from South and North America, Europe, Asia and Australia. A dramatic increase of NAFLD prevalence up to 80%, with a male-to-female ratio of 2 : 1, was observed in obese children from industrialized countries. Simple steatosis has often a benign clinical course in children, whereas NASH may progress to severe liver damage (i.e. cirrhosis) increasing liver-related morbidity and mortality, even if the natural history of paediatric NAFLD remains scarcely documented. On the contrary, it is widely demonstrated that children with NAFLD can display several features of metabolic syndrome increasing the risk for type 2 diabetes and cardiovascular disease.
In this epidemic scenario, and in view of its primary origin, paediatric NAFLD represents an optimal model to identify risk factors and pathogenetic mechanisms that lead to development and progression of the disease. The comprehension of factual origins for NAFLD in children is crucial to discover appropriate diagnostic and therapeutic approaches.
In this review, we discuss recent evidence on histological pattern, risk factors, pathogenesis of severe organ damage, diagnosis and treatments in paediatric NAFLD.