What is alcoholic liver disease? Alcoholic liver disease is a toxic liver injury caused by long-term heavy alcohol consumption, initially hepatocellular steatosis, then hepatitis p liver fibrosis, and eventually cirrhosis. How alcohol is metabolized in the body After drinking alcohol, more than 80% of ethanol is rapidly absorbed by the gastrointestinal tract and only 2%-10% is excreted from the kidneys and lungs, and the liver is the only organ that metabolizes ethanol in the body. Ethanol is metabolized by two pathways: 1) in the hepatic cytoplasm, ethanol is transformed into acetaldehyde by ethanol dehydrogenase (ADH); 2) ethanol is transformed into acetaldehyde by the action of the ethanol oxidation system (MEOS) in the microsomes of hepatocytes. Then it is further metabolized to acetic acid in mitochondria, which is transformed into acetyl coenzyme A by transporting extrahepatic tissues with hepatic blood flow , entering the tricarboxylic acid cycle, and finally oxidized to carbon dioxide and water. Third, the occurrence of alcoholic liver disease factors 1, daily alcohol intake: the safe amount of alcohol intake is still controversial, the Royal College of Physicians recommended amount: <210g/week for men and <140g/week for women. Italian prospective studies suggest that the risk value for the occurrence of ALD is 30g of alcohol intake per day, and the risk increases with the increase of intake. 2.Gender and cumulative time: women are more prone to ALD, in general the average alcohol consumption exceeds 80g per day, connected with 10 years to develop, and the intake threshold for women is 2/3 of the above total. 3.Genetic factors. 4, drinking mode: drinking alcohol on an empty stomach and drinking large amounts of alcohol for a short period of time. Those who drink alcohol on an empty stomach with high alcohol concentration will have more alcohol absorption in the intestine and higher alcohol concentration in the blood. 4. Clinical types of alcoholic liver disease The three most common types are alcoholic fatty liver, acute alcoholic hepatitis and alcoholic cirrhosis. Fatty liver occurs in at least 80% of heavy drinkers, alcoholic hepatitis occurs in 10%-35%, and cirrhosis can occur in nearly 10%. They are the three steps in the development of alcoholic liver disease. 1. Alcoholic fatty liver: Alcohol can promote the synthesis of triacylglycerol in the liver, increase the mobilization of surrounding adipose tissue, release fatty acids, enter the liver with blood flow, and accelerate the synthesis of triacylglycerol. Due to the accumulation of triacylglycerol in the liver, fatty liver is formed. Liver steatosis is inevitable when the daily alcohol intake exceeds 80g, and triacylglycerol droplets of different sizes are visible in the cytoplasm of damaged liver cells. Liver function is generally normal, the disease is reversible after abstinence from alcohol, continued excessive alcohol consumption can make the disease further develop into liver fibrosis, death due to fatty liver is less common. 2, acute alcoholic hepatitis: the toxic effects of acetaldehyde and a large number of free radicals generated during the oxidation of ethanol can damage hepatocytes, causing hepatocyte degeneration and necrosis, hepatocyte balloon-like changes, the appearance of ethanol (Mallory) transparent vesicles. Antigens and antibodies to ethanol hyaline vesicles can be measured in the patient's serum, and the level of antibodies parallels the degree of disease progression; when antibody levels remain positive, the disease can progress to cirrhosis. It is estimated that alcoholic hepatitis can develop after 15-20 years of excessive alcohol consumption. Even if the patient abstains from alcohol the disease can still progress and the death rate can exceed 30%. 3, alcoholic cirrhosis: the risk of alcoholic cirrhosis is significantly higher in people who continue to drink a lot of alcohol, often manifested as small nodular cirrhosis, collagen deposition in the interstitial space, and around the central vein to form fibrosis, the confluent area and the central vein between the fibers separating hepatocytes to form regenerative nodules, can quickly develop into cirrhosis, more serious in women. 1-year survival rate is 60% to 70%, 5-year survival rate is 35 The 1-year survival rate is 60% to 70% and the 5-year survival rate is 35 to 50%. V. What are the clinical manifestations of alcoholic fatty liver? The patient is in good nutritional status and has a fat body. Generally asymptomatic or with only mild discomfort, such as generalized lethargy, easy fatigue, loss of appetite, etc. Further development of the disease may include nausea, vomiting, jaundice, liver enlargement and pain in the liver. In a few cases, the disease may be complicated by Zieve syndrome, which is a triad of hyperlipidemia, hemolytic anemia and jaundice. Liver function: mild to moderate elevation of transaminases (ALTASL), AST is often higher than ALT. serum bilirubin may be increased but is often 170umol/l. serum albumin is decreased and globulin is increased. There may be anemia and elevated white blood cells. The manifestations of alcoholic cirrhosis are similar to those of non-alcoholic cirrhosis, such as loss of appetite, fatigue and weakness, chronic low fever in the early stage. In the late stage, jaundice, ascites and portal hypertension may appear as a result of liver function loss. Liver palms, spider nevus, enlarged parotid glands, gynecomastia, splenomegaly and ruptured esophageal varices may be seen. Onset is around 50 years of age and death is often due to complications around 60 years of age. Liver function: decreased serum albumin, increased globulin, inverted white/sphere ratio, and varying degrees of decreased red blood cells, white blood cells and platelets. Seven, how to determine the prognosis of alcoholic liver disease Discriminant power value (DF) can predict the prognosis of short-term alcoholic hepatitis. df=4.6[(PT-normal control)+serum bilirubin level/17.1]. df>32 predicts severe disease and 50% death within 2 months. wbc and bpc decrease, either secondary to hypersplenism or due to direct alcohol toxicity. Ultrasonography can detect alcoholic fatty liver and hepatitis by echogenic changes. Liver biopsy is important to clarify the severity of liver injury and provide prognostic indicators. Serum transaminase levels are elevated, and the AST/ALT ratio may be more than twice as high, excluding viral hepatitis and autoimmune diseases when ALT is significantly elevated. r-GT is moderately to significantly elevated. ALTAST r-GT can be significantly decreased after more than 4 weeks of abstinence from alcohol. In severe alcoholic liver disease, serum bilirubin level is significantly elevated. How to treat alcoholic liver disease The most important thing for the treatment of alcoholic liver disease is strict abstinence from alcohol, proper rest, and giving enough calories (10.5-12.6 kJ per day), vitamins and proteins. After 3-6 weeks of abstinence from alcoholic fatty liver disease, the fat in the liver can disappear. In other types of alcoholic liver disease, early abstinence from alcohol can prolong life and reduce the death rate. Select appropriate hepatoprotective drugs to prevent hepatocyte necrosis liver fibrosis and inflammatory response. 1.Curel health (carnitine): it can promote the oxidative metabolism of fatty acids and is more effective in treating fatty liver. 2, antioxidants: reduced glutathione vitamins, etc. may reduce lipid peroxidation damage to liver cells, to prevent liver fibrosis. 3, lipid-lowering drugs: hyperlipidemia can be used appropriately, such as fenofibrate Gefirox and other drugs mainly to reduce triacylglycerol, but also to reduce cholesterol; pravastatin simvastatin and other drugs mainly to reduce cholesterol, while reducing triacylglycerol. Lipid-lowering drugs have certain adverse reactions that cause liver damage, and attention should be paid to the follow-up of liver function during the use of drugs. 4, foreign reports ursodeoxycholic acid is effective in the treatment of fatty liver. Other trials include cholinesterone tablets, etc. For patients with advanced cirrhosis, liver transplantation can be considered if the liver function does not improve significantly after more than six months of abstinence from alcohol.