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Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide. It represents a spectrum of disease from simple hepatic steatosis to steatohepatitis that may develop into progressive hepatic fibrosis and even cirrhosis. NAFLD is the most rapidly increasing indication for liver transplantation in adults. In children, the incidence of NAFLD has also increased over the past decade. Although the majority of children with NAFLD are overweight or obese, there is an increasing subset of children with normal body mass index with so-called lean NAFLD. NAFLD in children is associated with several extrahepatic manifestations, including hyperlipidemia, insulin resistance, and obstructive sleep apnea. The pathogenesis of NAFLD in children involves a multifactorial interaction among genetics, in utero exposures, early childhood exposures, and ongoing nutritional exposures. Although there are some similarities between pediatric NAFLD and adult NAFLD, liver biopsies in children show histologic differences between the two. The current standard-of-care treatment of NAFLD in children is lifestyle change to decrease caloric intake and increase physical activity. There are no medications currently approved for the treatment of NAFLD in children. This article aims to summarize the current understanding of pediatric NAFLD and future directions for intervention and therapeutic aims. [ABSTRACT FROM AUTHOR]

Abstract Background Hepatic steatosis is a common manifestation of CF-related liver disease(CFLD). Controlled attenuation parameter(CAP) measurement during transient elastography(TE) semiquantifies liver steatosis. We examined the relationship between CAP and CFLD severity, clinical factors and liver stiffness measurements(LSM). Methods This is a cross-sectional study of CF patients seen for outpatient care between January 2013–March 2014. CFLD severity was categorized as no CFLD, CFLD without portal hypertension(PHTN) and CFLD with PHTN, based on published criteria. Results 129 patients (median 18.4y; 57% male) had valid CAP. 70(54%) had no CFLD, 44(34%) CFLD without PHTN, and 15(12%) CFLD with PHTN. The median CAP was 210 dB/m (IQR 181–239). Steatosis(CAP ≥230 dB/m) was seen in 27% of subjects without CFLD, 48% in CFLD but no PHTN, and 20% in with CFLD and PHTN(P =.04). CAP was higher for subjects with CFLD without PHTN (P <.05). There was no CAP difference between subjects with no CFLD and those with CFLD and PHTN (P ≥.65). LSM was not different between no CFLD and CFLD without PHTN (P =.07), but each of these groups had lower LSM compared to subjects with CFLD and PHTN(P <.001 for each). Except for direct bilirubin, CAP was not associated with clinical markers of liver disease. Conclusion CAP was normal in 86(67%) of patients with CF and was not associated with standard clinical markers of liver disease. CAP was higher in patients with liver disease, which could possibly reflect the loss of steatosis observed with progression to cirrhosis and portal hypertension. Highlights • CAP is a non-invasive tool to assess liver steatosis. • CAP was normal in a majority of children/young adults with Cystic Fibrosis. • CAP is higher in patients with CFLD without portal hypertension. [ABSTRACT FROM AUTHOR]