Alcoholic liver disease has a variety of manifestations, the initial stage is usually manifested as fatty liver, and then can develop alcoholic hepatitis, alcoholic liver fibrosis and alcoholic cirrhosis, in severe alcohol abuse can induce extensive hepatocellular necrosis or even liver failure. Alcoholic liver disease clinical diagnostic criteria 1, a history of long-term drinking, generally more than 5 years, equivalent ethanol alcohol amount > 40g / d, women ≥ 20g / d; or a history of heavy drinking within 2 weeks (> 80g / d). 2.After abstinence from alcohol, serum AL T, AST and GGT decreased significantly, and basically returned to normal within 4 weeks, i.e., below 2 times the upper limit of normal (ULN). The enlarged liver shrinks significantly within 1 week and basically returns to normal within 4 weeks. 3. When diagnosing, attention should be paid to the combination of HBV or HCV infection, excluding metabolic abnormalities and drug-induced liver injury. If the above conditions are not met, histological evidence of diagnosis should be obtained. The following items can be used as diagnostic reference: AST/AL T > 2, elevated serum glycodeficiency transferrin (CDT), elevated mean red blood cell volume (MCV), positive alcoholic hepatocyte membrane antibody, serum glutamate dehydrogenase (GDH) / ornithine carbamyltransferase (OCT) > 0.6, and increased liver volume (> 720 cm3/m2 body surface area) measured by early CT. It should be noted that alcoholic liver disease can occur even if the equivalent ethanol consumption is < 40 g/d when genetic susceptibility is present. The formula for converting the amount of ethanol is: g = amount of alcohol consumed (ml) × alcohol content (%) × 0.8 (specific gravity of alcohol). The clinical typing diagnosis of alcoholic liver disease for those who meet the clinical diagnostic criteria of alcoholic liver disease is as follows: 1. mild alcoholic liver disease: those who have a history of long-term alcohol consumption, but the liver function test is basically normal and the liver histological performance is consistent with mild alcoholic liver disease. 2. 2. Alcoholic fatty liver: diagnosed by imaging (CT or B ultrasound) with specific manifestation of fatty liver or confirmed by pathology. 3. Alcoholic hepatitis: without biopsy, 3 or more of the following diagnostic bases and additional items should be met. Diagnosis: (1) increased alcohol consumption as a trigger for the onset or worsening of the disease; (2) elevated AST-based serum aminotransferases; (3) elevated serum bilirubin (> 34.2 μmol/ L). Additional items: (1) right upper abdominal distension; (2) fever; (3) increased peripheral blood leukocytes; (4) increased AL T > 2. 0ULN; (5) increased GGT > 2. 0ULN. Severe alcoholic hepatitis may be combined with hepatic encephalopathy and decreased prothrombin activity (< 40%) and other manifestations of liver failure. 4.Alcoholic cirrhosis: those with clinical manifestations of cirrhosis should be differentiated into compensated and decompensated in the diagnosis. 3, alcoholic liver disease pathology diagnostic criteria 1, mild alcoholic liver disease: several basic lesions of alcoholic liver disease can be seen in the liver, but the degree is light. 2.Alcoholic fatty liver: steatosis occurs in > 30% of hepatocytes in the liver lobules, and is classified as mild, moderate or severe according to the extent of steatosis. Fatty liver cells up to 30%-50% are mild, 50%-75% are moderate, >75% are severe, fatty changes are mainly large vesicular, occasionally fatty granulomas. A small number of alcoholics may develop small vesicular steatosis. Mild steatosis can disappear after 2-4 weeks of abstinence from alcohol. 3, alcoholic hepatitis: hepatocytes are balloon-like and hyaline, and Mallory vesicles are seen in the cell pulp. Sometimes huge mitochondria, intrahepatocellular siltation, small bile duct hyperplasia and iron particle deposition are seen. Neutrophilic leukocytes infiltrate the foci of inflammation and necrosis, and apoptotic vesicles are easily seen, and the necrosis may fuse. It may be accompanied by different degrees of steatosis and fibrosis. According to the extent and distribution of inflammatory necrotic foci, they can be divided into mild, moderate and severe. Mild: necrotic foci are mainly seen in the 3 bands; moderate: inflammatory necrotic foci are significantly increased, not limited to the 3 bands, the surrounding common balloon-like changes or transparent degeneration of hepatocytes, the cytoplasm of Mallory vesicles can be seen; severe: on the basis of chronic alcoholic hepatitis lesions occur in the hepatocytes diffuse degeneration, necrosis and cholestasis, mostly seen in the short-term history of heavy alcohol consumption. 4, alcoholic liver fibrosis: perihepatocellular fibrosis and perivenous fibrosis are common, and severe cases can lead to terminal venous occlusion. Fibrosis in the confluence area extends to the surrounding area to form stellate fibrosis, which can develop into a fibrous septum, with or without steatosis and inflammation. The degree of fibrosis can be classified as mild, moderate or severe. Mild: perihepatocellular fibrosis is seen in the 3 bands or spread to the 2 bands, with a few fibrous septum formation and preservation of lobular structure; moderate: increased fibrous septum, extensive perihepatocellular and perivenous fibrosis, resulting in disorganization of lobular structure; severe: early and sometimes extensive perivenous fibrosis is seen, with the formation of vascular fibrous septum along the 3 bands containing dilated blood sinusoids, separating the lobules into tiny nodules, with the regeneration of nodules alteration With the regeneration of the nodules, the nodules gradually develop into the typical small nodular cirrhosis. 5.Alcoholic cirrhosis: early nodules are very small, late regenerative nodules increase in size and are clearly defined and surrounded by dense fibrous tissue. Sometimes hepatocyte lipid changes or iron particle deposition are seen in the nodules. According to the presence or absence of active inflammation in the liver, cirrhosis is also divided into active and inactive.