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      Nonalcoholic fatty liver disease: a challenge for pediatricians.

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          Abstract

          Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome and is considered the most common form of chronic liver disease in children. Several factors contribute to NAFLD development, including race/ethnicity, genetic factors, environmental exposures, and alterations in the gut microbiome. The histologic spectrum of NAFLD ranges from simple steatosis to the more aggressive nonalcoholic steatohepatitis (NASH). Fibrosis and eventually cirrhosis can develop from NAFLD during childhood. Diagnosing advanced disease is challenging and may require a liver biopsy, highlighting the urgent need for reliable, noninvasive markers of disease severity. The mainstay of treatment for NAFLD remains lifestyle modifications and weight loss. Probiotics and ω-3 fatty acids may ameliorate disease progression. Recent data have suggested that vitamin E may be considered as a NASH-specific therapy in children, and there are several ongoing human studies evaluating different therapeutic targets for NAFLD. We provide an up-to-date review of the risk factors, diagnosis, and treatment to manage this common disease in children.

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          Author and article information

          Journal
          JAMA Pediatr
          JAMA pediatrics
          2168-6211
          2168-6203
          Feb 2015
          : 169
          : 2
          Affiliations
          [1 ] Hepato-Metabolic Disease Unit, Bambino Gesù Children's Hospital, Italian Scientific Institute for Research and Care, Rome, Italy.
          [2 ] Department of Pediatric Gastroenterology and Hepatology, Cleveland Clinic Children's Medical Center, Cleveland, Ohio.
          [3 ] Paediatric Liver, Gastrointestinal, and Nutrition Centre, King's College London School of Medicine, King's College Hospital, London, England.
          Article
          2022277
          10.1001/jamapediatrics.2014.2702
          25506780
          ed8c855b-ac71-47f0-b285-ed4ff0862280
          History

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