Alcoholic liver disease

　　The triggering factor of this disease is first and foremost alcohol consumption. The liver is the largest detoxification organ in the human body. After drinking, more than 90% of ethanol is metabolized in the liver. A small amount of ethanol is converted into acetaldehyde after dehydrogenation or oxidation, enters the mitochondria for dehydrogenation to form acetic acid, and is then degraded into water and carbon dioxide in peripheral tissues, that is, after detoxification and metabolism by the liver, it becomes a non-toxic substance and is excreted from the body. However, the intermediate metabolite acetaldehyde has strong liver toxicity, binds to proteins, and through direct and induced immune or inflammatory reactions, damages liver cells, leading to metabolic disorders in the liver, which is the main cause of alcoholic liver disease.

　　A secondary factor is malnutrition. Long-term alcohol consumption leads to weakened function and digestive and absorptive disorders of the pancreas and small intestine. Due to reduced absorption of antioxidants in food, an increase in the production of pro-oxidants, and a decrease in antioxidants, oxidative stress is easily caused, which further aggravates the damage and death of liver cells, leading to malnutrition.

　　The third factor is that some alcoholic liver diseases are also due to heredity. The enzymes and cytochromes involved in ethanol metabolism have genetic polymorphisms, that is, the individual differences in ethanol metabolism rate are related to gene regulation, but the specific genetic markers have not been determined.

　　The last factor is gender. The activity of alcohol dehydrogenase in the female gastrointestinal tract is lower than that in males, so the metabolism of ethanol is lower in females, and the concentration of ethanol in the blood is higher, making females more susceptible to alcoholic liver disease than males.

　　Alcoholic liver disease not only affects the synthesis and absorption of proteins and vitamins (malnutrition), but malnutrition also becomes a secondary factor for further damage to liver cells, which interact with each other, ultimately leading to the occurrence of fatty infiltration, inflammation, necrosis, and liver cirrhosis of liver cells. If left to develop, the occurrence of liver fibrosis and liver cirrhosis is inevitable, and many complications may also occur. These complications are often risk factors for the death of alcoholic liver disease:

　　1. Upper Gastrointestinal Bleeding:The portal hypertension caused by alcoholic liver disease often leads to upper gastrointestinal bleeding, and may also be due to acute gastric erosion, ulcer disease, or esophageal variceal rupture bleeding (EVB). If not handled and responded to in a timely and effective manner, it may lead to situations such as shock, which is a crisis to life, and the risk of death is relatively high.

　　2. Hepatic Encephalopathy:Alcoholic liver disease patients often suffer from gastrointestinal bleeding, electrolyte and acid-base imbalance, secondary infection, and other factors due to the complex pathogenesis of the disease itself. If not treated properly or in a timely manner during the occurrence of hepatic coma, the mortality rate is extremely high. For alcoholic liver disease patients, it should start with the prevention of the above triggering factors and actively treat alcoholic liver disease.

　　3. Ascites and Infection:Alcoholic liver disease leads to the accumulation of large amounts of ascites due to factors such as electrolytes, osmotic pressure, and nutrition, similar to ascites in patients with liver cirrhosis and liver cancer. This leads to a vicious cycle, making it easy to develop electrolyte imbalance or threaten the entire system, leading to death. At the same time, due to nutritional and various complications during the course of alcoholic liver disease, the immune system is weakened, making it easy to get infected, especially with pulmonary infections and bacterial spontaneous peritonitis. The incidence of pneumonia is 3-4 times higher than that in the general population, and it is one of the important causes of death, so it should be paid attention to in prevention and treatment.

　　4. Electrolyte disorder and acid-base imbalance:Ethanol metabolism produces hyperlactatemia and ketosis, leading to metabolic acidosis of AG (anion gap), and excessive alcohol sedation can cause respiratory acidosis; excessive breathing in alcohol withdrawal syndrome can cause respiratory alkalosis. At the same time, due to less intake, more excretion, poor absorption of gastrointestinal tract and renal tubules, and acid-base disorder caused by alcohol, electrolyte disorder occurs, leading to hypokalemia, hypomagnesemia, hypocalcemia, and hypophosphatemia, which are important causes of death.

　　Early alcoholic liver disease may not show any symptoms, but the liver has pathological changes. There is often a history of heavy drinking in a short period of time before onset, with significant weight loss, loss of appetite, nausea, vomiting, general fatigue and weakness, fever, abdominal pain, and diarrhea, upper gastrointestinal bleeding, and mental symptoms.

　　Common symptoms of alcoholic liver disease:Liver enlargement and tenderness caused by fat infiltration; jaundice, nausea, and vomiting due to liver cell necrosis; portal hypertension and complications, such as splenomegaly, esophageal varices, and ascites; other symptoms, such as spider nevus and liver palms, etc.

　　Symptoms of advanced alcoholic liver disease:The basic symptoms of advanced alcoholic liver disease are liver pain, general weakness, poor digestion, loss of appetite, nausea and vomiting, fever, abdominal distension and diarrhea, etc.; serious symptoms include upper gastrointestinal bleeding and mental symptoms, portal hypertension and complications, such as splenomegaly, esophageal varices, ascites, spider nevus, and liver palms, etc.

　　According to incomplete statistics, the incidence of alcoholic liver disease is increasing year by year, and its degree of lesions is proportional to the total amount of alcohol intake. Alcoholic fatty liver is an important type of alcoholic liver disease and fatty liver, with隐匿发病 and a high incidence, and can develop into alcoholic hepatitis and even liver cirrhosis. It is recommended to focus on prevention for alcoholic fatty liver, including moderate drinking (abstaining from alcohol), improving nutrition, preventing liver damage, and preventing or reversing the progression of liver fibrosis. Experts suggest that the following aspects should be addressed for prevention and treatment in daily life:

　　1. Moderate drinking:Moderate drinking is beneficial to health, the key is to control the amount of alcohol intake. Alcohol has a strong toxicity to liver cells, 95% of alcohol directly affects protein and fat metabolism, thus reducing the liver's detoxification ability, leading to alcoholic fatty liver. Once alcoholic liver disease occurs, alcohol must be absolutely prohibited during the treatment process and after the recovery of the disease, regardless of which stage it is.

　　2. Reasonable diet:The principle should be to eat a lot of vegetarian foods and grains, with a combination of coarse and fine, preference for light flavors, avoid greasy foods, rich in nutrition, easy to digest; eat small meals more often, avoid cold, sweet, spicy and痰-assisting dampness foods; eat more vegetables and fruits, consume dairy and beans regularly, light and low-salt diet, and pay attention to supplementing foods rich in vitamins B, C, K, and folic acid, such as fresh fruits and vegetables.

　　3. Regulate one's emotions:For those with alcoholic liver disease or the general population, maintaining a good mental state is crucial to prevent the exacerbation of the condition due to psychological stress and mental factors, which may affect the whole recovery process and therapeutic effect of the disease.

　　4. Combination of work and rest:For healthy individuals, attention should be paid to physical exercise, balancing body fat, and carrying out reasonable metabolism in a timely manner. For patients with alcoholic liver disease, attention should be paid to rest, keeping a regular lifestyle, and moderate work and rest. During the recovery process, appropriate exercise methods should be chosen according to the severity of the disease and the strength of the constitution.

　　5. Early detection and early treatment:Early detection and treatment of alcohol intoxication can prevent the occurrence of alcoholic liver disease. It is recommended to regularly go to the hospital for liver function and physical examination, especially for those who have been drinking for a long time or have liver or digestive system diseases.

　　6. The function of Schisandra chinensis:Adjuvant treatment for chemical liver injury, can be used to treat alcoholic liver disease, alcohol intoxication, fatty liver, and can be used for the prevention and maintenance of frequent drinkers and patients with liver disease.

　　7. Selenium supplementation for liver protection:Selenium is known as an important 'liver protector', supplementing selenium can reach normal levels of glutathione peroxidase activity in the liver, and plays a good role in nourishing and protecting the liver.

　　Clinical examination methods for alcoholic liver disease:

　　1. Plasma protein

　　Changes in total plasma protein and inversion of the albumin globulin ratio are the most common biochemical abnormalities, and some patients show increased α1, α2, and β globulins in plasma protein electrophoresis. After the fatty liver recovers, the abnormality of plasma protein recovers later than other indicators, taking 3 to 6 months to return to normal.

　　2. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST)
　　The former does not increase significantly, AST/ALT>2 has diagnostic significance, and the insensitivity of ALT increase is due to the reduction of the enzyme's active cofactor B6 caused by acetaldehyde. The inhibition of ALT activity in liver tissue is more significant than that of AST.

　　3. Gamma-glutamyltransferase (γ-GT)
　　Elevated when the liver cell mitochondria are damaged by alcohol, it is a relatively sensitive indicator for the diagnosis of alcoholic liver disease.

　　4. Alcoholic oral loading test
　　Detection of changes in glycoprotein, prealbumin, α2HS glycoprotein, and ceruloplasmin, which are all reduced in alcoholic fatty liver.

　　5. Ultrasound examination
　　Diffuse fatty liver under ultrasound can be divided into three types: mild fatty liver: characterized by enhanced near-field echo and不明显distant-field echo attenuation, visible intralobular tubular structures; moderate fatty liver: enhanced anterior field echo and attenuated posterior field echo, blurred tubular structures; severe fatty liver: significantly enhanced near-field echo and obvious attenuation in the distant field, unclear tubular structures, indistinguishable; the ultrasonic changes of focal fatty liver are non-uniform distribution, showing multiple strong echo nodules, but without mass effect. Liver biopsy can be performed if necessary.

　　6. CT examination
　　Its accuracy is better than that of ultrasound, mainly showing that the liver parenchyma density is generally or focally reduced.

　　Recommended dietary therapy for alcoholic liver disease:
　　1. Angelica, Curcuma, Hawthorn, and Pomelo Drink:Angelica sinensis and Curcuma longa each 12 grams, hawthorn and pomelo cake each 25 grams. Boil the above four ingredients with water and take the decoction. Take it in 2 to 3 doses.
　　2. Polygonatum Ganoderma Alisma Drink:Polygonatum odoratum, Ganoderma lucidum 15 grams, Citrus reticulata Blanco 10 grams, Rhizoma Cyperi 10 grams, Alisma orientale 6 grams. Boil the above ingredients in water to get the juice. Take 2-3 times.
　　3. Herba Lysimachiae Amomum Fish:Herba Lysimachiae, prei herba, Amomum villosum 10 grams, Carassius auratus 1 tail, salt, and ginger as appropriate. Remove the scales, gills, and internal organs of the Carassius auratus, and boil with the other three ingredients in water. Season with salt and ginger after the fish is cooked.
　　4. Fish Brain Powder:Appropriate amount of fish brain (or fish roe). Roast fish brain or fish roe to a golden brown, grind into fine powder. Take with warm water, 3-5 grams each time. Suitable for fatty liver.
　　5. Corn Silk Malva Verticillata Red Bean Soup60 grams of corn silk, 15 grams of malva verticillata, 100 grams of red bean, and appropriate amount of sugar. Boil corn silk and malva verticillata in water to get the juice, then cook the red bean into soup, add sugar for seasoning. Take 2 times, eat beans, and drink soup.
　　6. Atractylodes Jujube:Atractylodes macrocephala, prei herba, and Curcuma aromatica each 12 grams, jujube 120 grams. Wrap Atractylodes macrocephala, prei herba, and Curcuma aromatica in gauze, boil with water and jujube together, and try to make the jujube absorb the medicine liquid as much as possible, remove the dregs and eat the jujube.
　　7. Safflower Hawthorn Tangerine Peel Drink:Safflower 10 grams, hawthorn 50 grams, tangerine peel 12 grams. Boil the above three ingredients in water, and take the juice. Take 2-3 times.
　　

　　Routine treatment methods for alcoholic liver disease:
　　1. Abstinence from Alcohol Abstinence from alcohol is the most important measure for the treatment of alcoholic fatty liver, and attention should be paid to the prevention and treatment of withdrawal syndrome during the process of abstinence.
　　2. Nutritional Support Alcoholic fatty liver patients require good nutritional support, and high-protein, low-fat diets should be provided on the basis of abstinence from alcohol, and attention should be paid to the supplementation of vitamins B, C, K, and folic acid.
　　3. Drug Treatment If serum ALT, AST, or GGT levels are slightly elevated, consider the use of medication. S-adenosylmethionine treatment can improve the clinical symptoms and biochemical indicators of alcoholic fatty liver patients; polyene phosphatidylcholine has a tendency to prevent histological deterioration in alcoholic fatty liver patients; drugs such as glycyrrhizin preparations, silymarin, polyene phosphatidylcholine, and reduced glutathione have varying degrees of antioxidant, anti-inflammatory, protective effects on liver cell membranes and organelles, and clinical application can improve liver biochemical indicators.