Alcoholic liver disease

Introduction to alcoholic liver disease Alcoholic liver disease is an alcoholic liver disease caused by long-term alcohol abuse, including fatty liver, alcoholic liver and alcoholic cirrhosis. The disease is more common in Western countries, 80% to 90% of the cause of liver cirrhosis is caused by drinking, in China, the importance of liver cirrhosis caused by hepatitis, the lack of attention to alcoholic cirrhosis is not enough. With the increase in the consumption of wine in China, the clinical manifestations of alcoholic liver disease have increased year by year, which is worthy of attention in the future. basic knowledge Sickness ratio: 5-8% Susceptible people: heavy drinkers Mode of infection: non-infectious Complications: cirrhosis, malnutrition, anemia, spider sputum, neuritis

Cause of alcoholic liver disease

There are many factors affecting the progression or aggravation of alcoholic liver injury. The risk factors that have been found in domestic and international research include: alcohol consumption, drinking years, alcoholic beverages, drinking patterns, gender, race, obesity, hepatitis virus infection, genetic factors. , nutritional status, etc. According to epidemiological survey data, liver damage caused by alcohol has a threshold effect, that is, reaching a certain amount of alcohol consumption or drinking years, it will greatly increase the risk of liver damage. However, due to the large individual differences, studies have shown that the dose-response relationship between drinking and liver damage is not very clear.

Alcohol (25%):

There are many varieties of alcoholic beverages, and the damage caused by different alcoholic beverages to the liver is also different. Alcoholic drinking is also a risk factor for alcoholic liver injury. Fasting drinking is more likely to cause liver damage than drinking with meals. Women are more sensitive to alcohol-mediated hepatotoxicity, and heavier alcoholic liver disease may occur in smaller doses and shorter drinking periods than men. Drinking the same amount of alcoholic beverages, the levels of alcohol in the blood of men and women are significantly different.

Gene (15%):

The allele frequency and genotype distribution of alcoholic liver disease susceptibility genes alcohol dehydrogenase (ADH) 2, ADH3 and aldehyde dehydrogenase (ALDH) 2 in the Han population are different from those in Western countries, and may be Chinese alcoholics and One of the reasons for the incidence of alcoholic liver disease is lower than in Western countries.

Genetics (20%):

Not all drinkers have alcoholic liver disease, but only in a small group of people, indicating that there are individual differences between groups in the same region. The rise in the mortality rate of alcoholic liver disease is related to the degree of malnutrition. The lack of vitamin A or the decrease in vitamin E levels may also aggravate liver damage. Diets rich in polyunsaturated fatty acids can contribute to the progression of alcoholic liver disease, while saturated fatty acids protect against alcoholic liver disease. Obesity or overweight can increase the risk of progression to alcoholic liver disease. Hepatitis virus infection and alcohol have a synergistic effect on liver damage. Drinking alcohol based on hepatitis virus infection or HBV or HCV infection based on alcoholic liver disease can accelerate the occurrence and development of liver disease.

Pathogenesis

In recent years, the pathogenesis of alcoholic fatty liver has been proven:

1. Free fatty acid enters the blood too much.

2. The new synthesis of fatty acids in the liver increases.

3. Oxidation of fatty acids in the liver is reduced.

4. Triacylglycerol is too synthetic.

5, lipoprotein release disorders in liver cells.

It is currently believed that the direct toxic effect of alcohol on hepatocytes is the main cause of fatty liver.

The pathogenesis of alcoholic hepatitis has been shown to be involved in immune factors in recent years, and it is of great significance. It is currently believed that swollen hepatocytes cannot discharge filaments and accumulate in hepatocytes to form alcoholic transparent bodies and cause transparent bodies. The production of antibodies, self-hepatic antigens and isolated alcoholic transparent bodies, can stimulate lymphocyte transformation and migration-moving inhibitory factor (MIF) activity in patients.

Alcoholic cirrhosis can detect autoimmune characteristics of natural DNA antibodies, and liver cell membranes produce IgG and IgA antibodies, which can be adsorbed by liver infusion.

In recent years, it has been proved that alcohol and acetaldehyde can change liver cell membrane antigen, and it is not directly affected by the toxicity of acetaldehyde on the liver cell membrane.

Alcoholic liver disease prevention

1, primary prevention

Not drinking alcohol-containing beverages is fundamental to prevent alcoholic liver disease. In real life, it is impossible to do this completely. Therefore, the second best thing is to ask for the least drink. After drinking alcohol, supplement the high-protein and high-vitamin diet and take hangover drugs such as Pueraria.

2, secondary prevention

For patients with heavy drinking and/or long-term drinking, liver function should be checked regularly, liver biopsy should be performed if necessary, alcoholic liver disease should be detected early, and the degree of development should be determined. There is still no specific diagnosis for alcoholic liver disease. , sensitive indicators, pending further research, early treatment of alcoholic liver disease include:

(1) Lifetime alcohol ban.

(2) high protein and high vitamin diet, especially vitamin B, vitamin A, C, K, etc., should be given a lot of folic acid.

(3) It has been reported that adrenocortical hormone is effective for fatty liver and active alcoholic hepatitis, but there are reports that the effect is not certain.

(4) The propylthiouracil has been tried and the effect cannot be determined.

Alcoholic liver disease complications Complications cirrhosis malnutrition anemia spider neuritis

In addition to general cirrhosis, there are malnutrition, anemia, spider mites, liver palm, neuritis, muscle atrophy, parotid swelling, male milk female, testicular atrophy.

Alcoholic liver disease symptoms Common symptoms Nail is fan-shaped spider mites Alcoholic cirrhosis Liver lesions diffuse upper abdominal discomfort Wean liver Palm testicular atrophy Tongue inflammation Liver congestion

Alcoholic liver disease clinically divided into 3 types: fatty liver, hepatitis, cirrhosis, these three often mixed, the occurrence of liver disease and drinking time, the amount of drinking and nutritional status is positively correlated; drinking amount of less than 80g per day, liver Less damage, 160g / d for 11 years, 25% of cirrhosis; 210g / d for 20 years, 50% of cirrhosis, genetic formation of individuals have different sensitivity to alcohol, so alcoholic hepatitis and cirrhosis occur It is more common in HLA-B8 and B40.

1, fatty liver

Once a drink is close to drunk, liver fat can occur after a few hours, such patients are mostly moderate obesity, symptoms are insidious, similar to hepatitis gastrointestinal symptoms such as liver pain, upper abdominal discomfort, abdominal pain, etc. There are jaundice, edema, vitamin deficiency, liver, palpation soft, smooth and blunt, elastic or tender, less spleen enlargement, due to hepatocyte swelling and central venous hardening or venous embolism, can cause portal hypertension Ascites occurs, but there is no hardening. In severe cases, it may die due to hypoglycemia and fat embolism.

2, alcoholic hepatitis

Heavier gastrointestinal symptoms may have nausea, vomiting, loss of appetite, fatigue, weight loss, increased pain in the liver area, etc., severe cases of acute severe hepatitis or liver failure.

3, alcoholic cirrhosis

Europe and the United States account for 50% to 90% of total cirrhosis, which is rare in China, mostly in the age of 50, 80% have a history of drinking for a large amount of 5 to 10 years, in addition to general cirrhosis symptoms, malnutrition, anemia , spider mites, liver palm, neuritis, muscle atrophy, parotid gland enlargement, male milk female, testicular atrophy and other symptoms more common than hepatitis cirrhosis, and Dupuytren palm contracture, glossitis, parotid gland enlargement can be associated with the pancreas Inflammation, early liver, advanced liver shrinkage, splenomegaly is more common than hepatitis after liver cirrhosis, ascites appears earlier, often associated with ulcer disease.

Alcoholic liver disease check

Laboratory inspection

1, blood: there may be anemia, cirrhosis often have white blood cells and thrombocytopenia.

2, aspartate aminotransferase (AST) and alanine aminotransferase (ALT), increased in alcoholic hepatitis and active alcoholic cirrhosis, but AST increased significantly, ALT increased is not obvious, AST / ALT ratio is greater than 2 It has diagnostic significance for the above two diseases.

3, -glutamyltransferase (-GTP), distributed in the liver cell cytoplasm and capillary bile duct endothelium, alcohol is more sensitive to damage to liver cell microsomes.

4. The amino acid profile increases in proportion to -aminobutyric acid and leucine.

5, an abnormality of the indocyanine green retention test is an indicator of early alcoholic liver disease.

6, serum specificity, alcoholic transparent body, antigen-antibody positive, antigenic antibody positive in severe cases; recovery period antigen-negative, antibody is still short-term positive, if antigen-antibody positive indicates disease progression, serum IgA is elevated, and Low zincemia, high zincuria, so the rate of renal zinc clearance in liver disease can help diagnose the cause.

7, blood triglyceride and cholesterol increased to help the diagnosis of fatty liver, albumin decreased, globulin increased, prolonged prothrombin time contribute to the diagnosis of cirrhosis.

Film degree exam

1, B type ultrasound examination

(1) Fatty liver: It shows an increase in liver volume, a uniform appearance of fine echoes, and a "bright liver" with dense spots and enhanced sound beam attenuation.

(2) In alcoholic cirrhosis, the splenomegaly was enlarged, the echo of the liver parenchyma was enhanced, the tail leaf was relatively enlarged, and the diameter of the splenic vein and portal vein was significantly higher than normal (the former was 1.0 cm normal and the latter was 1.5 cm).

2, CT examination

(1) fatty liver: it is characterized by whole liver, liver leaf or local density is lower than that of spleen, and the normal liver area and spleen are obviously enhanced when scanning is enhanced, and the low density contrast with fatty liver area is more obvious.

(2) Liver cirrhosis: characterized by widening of the liver fissure, imbalance of the leaves of the liver and leaves, relative increase of the caudal lobe, deformation of the liver, enlargement of the spleen, greater than 5 rib units.

3, liver biopsy

Can determine the presence or absence of fatty liver, alcoholic hepatitis, cirrhosis, and can be identified by histological examination and other viral hepatitis.

(1) fatty liver: more than 1/3 of the liver lesions of the liver lobule (all liver cells more than 1/3) can be confirmed.

(2) Alcoholic hepatitis: its tissue features alcoholic transparent bodies (Mallory bodies), cell necrosis with neutrophil infiltration; balloon-like changes in liver cells.

(3) Alcoholic cirrhosis: typical cirrhosis is small nodular, no nodule area and central vein in the nodule, the size of the nodule is similar, and surrounded by fibrous septa, the diameter of the nodule is often less than 3mm, generally Not more than 1 cm, with the development of pathology can form large nodules or post-necrotic cirrhosis.

Diagnosis and identification of alcoholic liver disease

diagnosis

1, a long-term drinking history, generally more than 5 years, equivalent to ethanol male 40g / d, female 20 g / d, or a large number of drinking history within 2 weeks, equivalent to ethanol > 80 g / dt. However, attention should be paid to the influence of gender, genetic susceptibility and other factors. Ethanol amount (g) conversion formula = alcohol consumption (m1) X ethanol content (%) × 0.8.

2, the clinical symptoms are non-specific, can be asymptomatic, or have right upper quadrant pain, loss of appetite, fatigue, weight loss, jaundice, etc.; as the condition worsens, there may be neuropsychiatric symptoms and spider mites, liver palm and other performance.

3. Serum aspartate aminotransferase (AST), alanine aminotransferase (AL.T), gamma-glutamyltranspeptidase (GGT), total bilirubin (TBil), prothrombin time (PT), mean red blood cell volume (MCV) and hypoglycemic transferrin (CDT) and other indicators increased. Among them, AST/ALT>2, elevated GGT, and elevated MCV are characteristic of alcoholic liver disease, while CDT assay is more specific but not routinely performed. These indicators can be significantly reduced after the ban, and usually return to normal within 4 weeks (but GGT recovery is slow), which is helpful for diagnosis.

4, liver B-ultrasound or CT examination has a typical performance.

5, exclude hepatic virus infection and drugs, toxic liver damage and autoimmune liver disease.

Differential diagnosis

1, alcoholic fatty liver should be differentiated from obesity, drug, dystrophic fatty liver, diabetes and Reye sign often combined with fatty liver.

2, identification of drinking history with viral hepatitis, epidemiological history AST / ALT ratio > 1, specific serology, liver histology can be identified.

3, cholestatic alcoholic liver disease should be distinguished from surgical acute abdomen. The former often has elevated serum -GTP, AKP is elevated, and the liver can be significantly retracted after the liver is stopped drinking.

4, liver and liver cancer identification can check the fetal armor (AFP) or B-ultrasound, CT and so on.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.