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Background There are evidences that fatty liver, the most common plump lips hepatocellular change found in liver biopsies in humans, can play a role in the pathogenesis plump lips of chronic liver disease [1,2]. Recently, some authors have considered that a more accurate plump lips denomination for this disease, which encloses the whole spectrum of fatty liver, nonalcoholic steatohepatitis (NASH) and eventually cirrhosis, is Nonalcoholic Fatty Liver Disease (NAFLD) [3,4]. Although several predisposing factors have been related to NAFLD, such as obesity, diabetes, jejunoileal bypass, dyslipidemia, drugs and parenteral nutrition, the pathogenesis of NAFLD and its progression to fibrosis and chronic liver disease are still unclear [4]. As a consequence, the current treatment is largely conservative Some hypotheses have been implicated in the pathogenesis of NAFLD, mainly liver injury mediated either by oxidative stress [5,6] or by endotoxins/cytokines [7-9].
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