With the improvement of living standards and the increasing pace of modern life, various types of ethanol-containing beverages have gradually become in demand, and wine is a must at banquets, and some people have even become alcohol-dependent.
I. Concept.
Alcoholic liver disease is a liver disease caused by long-term heavy alcohol consumption. Initially, it usually appears as fatty liver, which can then develop into alcoholic hepatitis, liver fibrosis and liver cirrhosis. In severe alcohol abuse, extensive hepatocellular necrosis and even liver failure can be induced. This disease is one of the common liver diseases in China and is a serious health hazard to people.
Why can long-term heavy drinking cause liver disease? More than 95% of the ethanol consumed in the body after drinking is metabolized in the liver, and it is known that after entering the liver cells, ethanol is oxidized to acetaldehyde through three pathways: hepatic ethanol dehydrogenase, peroxisomal enzyme and hepatic microsomal ethanol oxidase system. Acetaldehyde has obvious toxic effects on hepatocytes, it is the main factor causing chronic progressive liver damage, resulting in impaired liver metabolism, in addition to fatty liver, hepatocyte degeneration and necrosis, complicated by inflammatory reactions, collagen fibers and nodular hyperplasia, which can eventually lead to cirrhosis.
II. Epidemiology
China still lacks national large-scale epidemiological survey data on alcoholic liver disease, but regional epidemiological surveys show that the number of people drinking alcohol and the prevalence of alcoholic liver disease in China are on the rise. From the early 1980s to the early 1990s, epidemiological surveys in northern China showed that the proportion of alcoholics in the general population rose from O, 21% to 14, 3%; at the beginning of this century, epidemiological surveys in southern and central and western provinces showed that the drinking population increased to 30, 9% a 43, 4%. Alcohol-related health problems can occur among alcoholics or excessive drinkers, with alcoholic liver disease being the most common organ damage caused by alcohol.
At the beginning of this century, the epidemiological survey data of alcoholic liver disease in southern and mid-western provinces showed that the prevalence of alcoholic liver disease in the adult population was alcoholic cirrhosis in the cause composition ratio of cirrhosis increased from 10,8% in 1999 to 24,O% in 2003. This shows that in China, alcohol-induced liver damage has become a problem that cannot be ignored and has become a major social and medical problem facing our country.
Third, risk factors
There are many factors that affect the progression or aggravation of alcoholic liver injury, and the risk factors that have been found in domestic and international studies include: the amount of alcohol consumed, the number of years of drinking, the variety of alcoholic beverages, the way of drinking, gender, race, obesity, hepatitis virus infection, genetic factors, nutritional status, etc.
According to epidemiological survey data, there is a threshold effect of liver damage caused by alcohol, i.e., the risk of liver damage increases greatly when a certain amount of alcohol is consumed or years of drinking are reached. However, due to large individual differences, there are also studies showing that the dose-effect relationship between alcohol consumption and liver damage is not very clear.
There are many varieties of alcoholic beverages, and the damage caused to the liver varies from one alcoholic beverage to another.
Drinking patterns are also a risk factor for alcoholic liver injury, and drinking on an empty stomach is more likely to cause liver injury than drinking with a meal.
Women are more sensitive to alcohol-mediated hepatotoxicity and may develop more severe alcoholic liver disease at smaller doses and shorter drinking periods than men. There is a significant difference in blood alcohol levels between men and women when consuming the same amount of alcoholic beverages. The reason for this may be twofold: one is that women have a lower average body weight than men and contain relatively less water and more fat in their bodies; therefore, drinking the same amount of alcohol, women have a higher blood alcohol concentration than men; the other is that women have lower ethanol dehydrogenase in their stomachs than men.
Race, genetics, and individual differences are also important risk factors for alcoholic liver disease. The allele frequencies of ethanol dehydrogenase (ADH)2, ADm and acetaldehyde dehydrogenase (ALDH)2 and the distribution of genotypes in the Han Chinese population are different from those in Western countries, which may be one of the reasons for the lower incidence of alcoholism and alcoholic liver disease in the Chinese population than in Western countries. Not all drinkers develop alcoholic liver disease, which occurs in only a small proportion of the population, suggesting that individual differences also exist between groups in the same region. More than two-thirds of severe alcoholics do not develop alcoholic hepatitis, and only 20-30% of those who develop it eventually develop cirrhosis, suggesting that susceptibility to alcoholic hepatitis is genetically related.
The increased mortality rate of alcoholic liver disease correlates with the degree of malnutrition. Vitamin A deficiency or decreased levels of vitamin E may also exacerbate liver damage. Diets rich in polyunsaturated fatty acids may promote the progression of alcoholic liver disease, while saturated fatty acids may be protective against alcoholic liver disease.
Obesity or overweight may increase the risk of progression of alcoholic liver disease.
Hepatitis virus infection and alcohol play a synergistic role in liver damage, and alcohol consumption on the basis of hepatitis virus infection or concomitant HBV or HCV infection on the basis of alcoholic liver disease can accelerate the development and progression of liver disease.
Four, alcoholic liver disease clinical diagnostic criteria
1, there is a history of long-term alcohol consumption, generally more than 5 years, equivalent ethanol amount ≥ 40g/d for men and ≥ 20g/d for women, but the influence of gender, genetic susceptibility and other factors should be noted. Amount of ethanol (g) = amount of alcohol consumed × ethanol content (%) × O, 8.
2, clinical symptoms are non-specific, may be asymptomatic, or have right upper abdominal distension and pain, loss of appetite, fatigue, weight loss, jaundice, etc.; with the aggravation of the disease, there may be neuropsychiatric symptoms and spider nevus, liver palm and other manifestations.
3.Serum glutamic oxalacetic transaminase, glutamic alanine transaminase, transpeptidase, total bilirubin, prothrombin time, mean red blood cell volume (MCV) and deficient glycotransferrin (cDT) are elevated. Among them, AST/ALT>2, elevated GGT, and elevated McV are characteristic of alcoholic liver disease, while CDT measurement, although more specific, is not routinely performed clinically. After abstaining from alcohol, these indicators can be significantly decreased, and usually return to normal within 4 weeks (but the recovery of transpeptidase GGT is slower), which helps to diagnose.
4. Ultrasonographic manifestations of the liver: diffuse fatty liver.
(1) Diffuse echogenicity enhancement in the near field of liver, with stronger echogenicity than kidney;
(2) Gradual attenuation of far-field echogenicity in the liver;
(Diagnosis by CT examination: diffuse liver density reduction, CT ratio of liver/spleen <1. Diffuse liver density reduction, CT ratio of liver/spleen <1,O but >O,7 is mild; CT ratio of liver/spleen ≤0,7 but >0,5 is moderate; C11 ratio of liver/spleen ≤O,5 is severe.
5. Exclude hepatophilic virus current infection as well as drugs, toxic liver injury and autoimmune liver disease, etc. Alcoholic liver disease can be diagnosed by meeting items 1-3 and 5 or items l, 2, 4 and 5; alcoholic liver disease is suspected by meeting items l, 2 and 5 only. Those who meet item 1 and also have evidence of current viral hepatitis infection can be diagnosed as alcoholic liver disease with viral hepatitis.
For those who meet the clinical diagnostic criteria of alcoholic liver disease, the clinical typing diagnosis is as follows.
1, mild alcoholic liver disease: liver biochemical indexes, imaging and histopathological examination are basically normal or slightly abnormal.
2.Alcoholic fatty liver: imaging diagnosis meets the criteria of fatty liver, and serum ALT, AsT or GGT can be slightly abnormal.
3.Alcoholic hepatitis: It is a group of clinicopathological syndrome caused by massive necrosis of hepatocytes in a short period of time, which can occur with or without cirrhosis, mainly manifested as elevated serum ALT, AsT and significantly increased 11Bil, which can be accompanied by fever and elevated peripheral blood neutrophils. Severe alcoholic hepatitis refers to the manifestation of liver failure in patients with alcoholic hepatitis, such as impaired coagulation mechanism, jaundice, hepatic encephalopathy, acute renal failure, upper gastrointestinal bleeding, etc., often accompanied by endotoxemia.
4. Alcoholic cirrhosis: there are clinical manifestations of cirrhosis and changes in blood biochemical indicators.
V. Treatment
Treatment principles of alcoholic liver disease: abstinence from alcohol and nutritional support to reduce the severity of alcoholic liver disease; improvement of pre-existing secondary malnutrition and symptomatic treatment of alcoholic cirrhosis and its complications.
1. Alcohol abstinence.
Abstinence from alcohol is the most important basic measure for the treatment of alcoholic liver disease, and attention should be paid to the prevention and control of withdrawal syndrome during the process of abstinence from alcohol. In mild alcoholic liver disease not accompanied by cirrhosis, simple abstinence from alcohol can restore or near normal liver function. In severe cases, such as hepatic decompensation with hemorrhage and encephalopathy, the morbidity and mortality rate is very high even if the patient abstains from alcohol. Generally speaking, alcoholic hepatitis is a reversible lesion, and the development of the lesion can be stopped after quitting alcohol; if it has developed into cirrhosis, the lesion is irreversible, and the practical significance of quitting alcohol may not be great.
2.Nutritional support.
Patients with alcoholic liver disease need good nutritional support. A high-protein, low-fat diet should be provided on the basis of abstinence from alcohol, and attention should be paid to the supplementation of vitamin B, vitamin C, vitamin K and folic acid.
3.Drug treatment
(1) Glucocorticoids can improve the survival rate of patients with severe alcoholic hepatitis (those with encephalopathy or Maddrey index >32).
(2) Metadoxine can accelerate the removal of sprinkles from the serum and help improve the symptoms of alcoholism and behavioral abnormalities.
(3) Application of hepatoprotective and detoxifying drugs. Drugs such as adenosylmethionine, glycopyrrolate preparations, silymarin analogs, polyenylphosphatidylcholine, reduced glutathione and dicyclomine have different degrees of antioxidant, anti-inflammatory, and hepatocyte membrane and organelle protection. However, multiple anti-inflammatory and hepatoprotective drugs should not be applied simultaneously to avoid increasing the burden on the liver and causing adverse reactions due to drug interactions.
(4) The liver of patients with alcoholic liver disease is often accompanied by pathological changes of liver fibrosis, so anti-liver fibrosis treatment should be emphasized.
(5) Actively manage the complications of alcoholic cirrhosis (such as portal hypertension, esophagogastric fundic varices, spontaneous bacterial peritonitis, hepatic encephalopathy and hepatocellular hepatocellular carcinoma, etc.).
(6) Liver transplantation can be considered for patients with severe alcoholic cirrhosis, but patients are required to abstain from alcohol for 3-6 months prior to liver transplantation and have no severe alcoholic damage to other organs.
Prevention and prognosis
One point of prevention is better than ten points of treatment. Prevention is especially important for the occurrence of alcoholic liver disease. The important thing is to drink less or not to drink.
What is a safe amount of alcohol to drink? Because some people are extremely sensitive to alcohol, there is no one standard that fits everyone. The normal liver does not metabolize more than 130-180g of ethanol per day, but a daily intake of 80g of ethanol for a long period of time is also dangerous! For women ≤ 20g/d. The harm of alcohol clearing on the liver increases with the amount and the duration of drinking, the more alcohol is consumed and the longer it takes, the more severe the steatosis of the liver becomes. Daily drinking is more harmful than intermittent drinking, and drinking a large amount of alcohol at one time is more harmful than drinking small amounts of alcohol in small portions throughout the day. Drinking 40 to 80 grams of alcohol per day is the risk threshold for liver fibrosis and cirrhosis, and exceeding this threshold can significantly increase the incidence of liver fibrosis and cirrhosis. If alcohol is abstained and hospitalized in time, most of them can be recovered and the death rate can be reduced to less than 10%.
Alcoholic hepatitis is currently considered to have a high independent risk factor for death. According to the natural history of alcoholic liver disease studied by liver biopsy histology, the prognosis of patients with fatty liver was found to be the best, with a survival rate of 70% to 80% in 4-5 years; the prognosis of patients with alcoholic cirrhosis accompanied by alcoholic hepatitis was the worst, with a survival rate of 30% to 50% in 4-5 years.