A<unk>  is a form of chronic hepatitis that shares the histologic features of alcohol-induced hepatitis but is found in patients without prior history of alcohol abuse. Based on the severity of the disease<unk>  encompasses a range of disorders including mild steatosis, steatohepatitis, advanced fibrosis, cirrhosis, and less commonly fulminant hepatic failure. Risk factors for<unk><unk>  liver disease include obesity, diabetes mellitus type 2, hyperlipidemia, and sudden dramatic weight loss. The diagnosis of<unk>  should be considered in any patient presenting with elevated transaminases without any underlying condition or pathological process.<unk>  must be distinguished from steatosis and steatohepatitis due to secondary causes. These include various forms of malnutrition, drugs (eg, warfarin, methotrexate, amiodarone, glucocorticoids, synthetic estrogens, tamoxifen, and various antibiotic and antiviral agents), metabolic and genetic disorders (eg lipodystrophy, dysbetalipoproteinemia, and acute<unk>  liver of pregnancy), use of total parenteral nutrition, and gastric bypass and other weight loss surgeries.<unk>  is mostly seen in obese individuals but may be encountered in thin or normal weight patients. Insulin resistance is a core feature of<unk> , diabetes, obesity, and dyslipidemia.<unk>  can therefore be considered part of the insulin resistance (or metabolic) syndrome. Insulin resistance leads to accumulation of fat within hepatocytesvialipogenesis (and inhibition of lipolysis) and hyperinsulinemia. The pathogenesis of<unk>  and its progression to NASH appears to result from a two-step process, whereby an initial insult in the form of insulin resistance due to genetic and acquired factors leads to hyperinsulinemia and accumulation of fat within hepatocytes (steatosis). The steatotic liver is then vulnerable to further insult; hepatocellular injury and fibrosis may develop in the presence of oxidative stress and the proinflammatory activity of cytokines and similar agents. This leads to exacerbation of insulin resistance; further oxidative stress; and acceleration of inflammatory, degenerative, and fibrotic processes. The natural history of<unk>  is dependent on the stage of the disease. The prognosis of simple steatosis seems to be relatively benign, with a 1% to 2% risk of developing cirrhosis over 15 to 20 years. Patients with NASH and fibrosis can progress to cirrhosis, which can lead to end-stage liver disease; hepatic decompensation; or hepatocellular carcinoma, a rare, end-stage outcome. Imaging techniques can be helpful by showing steatosis, but liver biopsy is the only way to assess the severity of inflammation and fibrosis. The mainstay of treatment for<unk>  is lifestyle modifications and treatment of underlying risk factors such as obesity, diabetes mellitus type 2, and hyperlipidemia.
Non-alcoholic fatty liver disease
Alcoholic liver disease
Alcoholic hepatitis
Autoimmune hepatitis
Benign intrahepatic cholestasis
Primary biliary cirrhosis
Ischemic hepatitis
Fatty liver