Basic concept and classification of fatty liver Fatty liver (liver steatosis and fatty liver) is a pathological concept, which means that the fat content in the liver exceeds 5% of the wet weight of the liver, or more than 30% of liver biopsy hepatocytes have fatty changes and diffuse distribution in the whole liver. Depending on the size of the lipid droplets stored in the hepatocytes, there are large-vesicular and small-vesicular fatty liver types, and lipid-like deposition disease is a special type of small-vesicular fatty liver. The commonly described fatty liver mainly refers to chronic diffuse fatty liver with a predominantly large vesicular type. Fatty liver disease (FLD) is a clinical concept that refers to a clinical syndrome characterized by diffuse hepatocellular steatosis in the lobules of the liver, and includes simple fatty liver, steatohepatitis, and fatty cirrhosis. Alcoholic liver diseases (ALD) and non-alcoholic fatty liver disease (NAFLD). Hepatitis C, autoimmune liver disease and Wilson’s disease can also cause hepatic steatosis, but because the main body of the lesion is in the confluent area, there is a specific disease designation and it does not belong to the category of common fatty liver disease. Etiology There are numerous etiological factors and causative factors of fatty liver. 1, nutritional factors: such as obesity, pernicious malnutrition, starvation, cachexia, total parenteral nutrition, and severe anemia. 2, chemical factors: including yellow phosphorus, arsenic, copper, benzene, carbon tetrachloride, chloroform and other industrial toxins; tetracycline, valproate, acetaminophen, cyclopiperidine, corticosteroids, estrogens, nucleoside analogues and anti mitotic drugs, as well as chronic alcoholism. 3, endocrine metabolic factors: such as diabetes, hyperlipidemia, pregnancy, Cushing’s syndrome. 4, genetic factors: including Wilson’s disease, lack of beta lipoproteinemia, galactosemia, glycogen accumulation disease, etc. 5 other: including HCV or HDV infection, inflammatory bowel disease, pancreatic disease, AIDS. Among them, obesity, type 2 diabetes, and alcoholism are the main current causes of fatty liver. However, the cause of 20% of fatty liver is still difficult to define. Clinical manifestations The clinical manifestations of fatty liver are mainly related to its etiology, pathological type and its accompanying disease states. It includes the symptoms of fatty liver itself, the manifestations of the primary underlying disease, and the complications of fatty liver, especially fatty cirrhosis and liver cancer. Fatty liver tends to occur in middle-aged and older men. The onset of the disease is insidious, and the clinical symptoms are mild and nonspecific, sometimes absent. Painless hepatomegaly occurs in more than 75% of cases. The detection rate of splenomegaly is less than 25%. Some patients occasionally feel vague pain in the liver, abdominal distension, fatigue, poor appetite and discomfort. The clinical manifestations of alcoholic liver disease are generally heavier than those of NAFLD, but subacute non-alcoholic steatohepatitis induced by obesity, post-empty ileal short-circuiting, and certain drugs is clinically significant, with rapid onset of decompensated cirrhosis and liver failure within six months. The clinical manifestations of focal steatohepatitis are mostly unremarkable due to the small extent of the lesions. Laboratory changes There are no ideal qualitative and quantitative laboratory indicators to reflect the presence or absence of fatty liver and its degree. In chronic fatty liver, ALT, AST, ALP, GGT and total bile acids may be mildly elevated, while transaminases are usually not elevated more than 2-4 times the upper limit of normal values. If serum aminotransferases are persistently elevated or significantly abnormal, steatohepatitis is indicated. Elevated bilirubin and prolonged PT reflect the severity of steatohepatitis. Combined testing of serum fibrosis indicators can reflect whether steatohepatic fibrosis and cirrhosis have been complicated. Serum AST/ALT2, AST, GGT and MCV are significantly elevated in over-nutritional fatty liver, as well as the ratio of glyco-deficient transferrin to total transferrin. In addition, detection of serum copperland protein and serum immunological and molecular biological markers of hepatitis virus can help in the differential diagnosis of steatohepatitis from Wilson’s disease and hepatitis B and C. Prognosis and regression The prognosis of acute small-vesicular steatohepatitis is similar to that of acute severe viral hepatitis, with a mortality rate of up to 60%. The prognosis for chronic large-vesicular fatty liver is relatively good, and non-alcoholic fatty liver in turn has a better prognosis than alcoholic fatty liver. Alcoholic fatty liver can progress directly to decompensated cirrhosis through central perivascular fibrosis or alcoholic hepatitis, and most patients die within 5 to 10 years from complications related to liver disease and occasionally from fat embolism, hypoglycemia, and severe pancreatitis. Focal fatty liver is not a health risk. The prognosis of post-hepatitis fatty liver depends mainly on the course of viral hepatitis itself, but concurrent obesity and diabetes mellitus can contribute to the progression of its liver disease.