Abstract:
© 2019 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd. Non-alcoholic fatty liver disease (NAFLD) covers conditions related to accumulation of fat in the liver if specific causes, such as significant alcohol consumption, long-term use of a steatogenic medication, or monogenic hereditary disorders can be excluded (WGO 2014). Non-alcoholic fatty liver disease features a wide spectrum of histologically conditions, from simple accumulation of fat ('fatty liver' or hepatic steatosis) to non-alcoholic steatohepatitis (NASH), liver fibrosis, and liver cirrhosis with clinical consequences (Brunt 2011; McPherson 2015; Bertot 2016). Simple hepatic steatosis is defined as when the fat, built up in the epithelial cells of the liver, is at least 5% of the liver weight, and the parenchymal cells and liver structure are intact. Non-alcoholic fatty liver (NAFL) is defined as the presence of hepatic steatosis with no evidence of hepatocellular injury in the formof ballooning of the hepatocytes. Non-alcoholic steatohepatitis is defined as the presence of hepatic steatosis and inflammation with hepatocyte injury (ballooning) with or without fibrosis (Brunt 2011). Nonalcoholic fatty liver disease is considered to be a clinical manifestation of the metabolic syndrome, that is the co-occurrence of metabolic risk factors for both type 2 diabetes and cardiovascular disease (abdominal obesity, hyperglycaemia, dyslipidaemia, and hypertension) (Dyson 2014;Mikolasevic 2016; AASLD NAFLD 2018). The prevalence of NAFLD is increasing, but only a small number of affected people develop inflammation, which may be followed by fibrosis and cirrhosis, possibly requiring liver transplantation (Bertot 2016; Younossi 2016). The life expectancy in people with hepatic steatosis is reported to be similar to the life expectancy of the general population (Lazo 2011).
