alcoholic fatty liver
Introduction
Introduction to alcoholic fatty liver Alcoholic fatty liver disease is a liver disease caused by long-term heavy drinking. It is a type of alcoholic liver disease. Have a long-term drinking history, generally more than 5 years, equivalent to ethanol male 40g / d, female 20g / d, or a large number of drinking history within 2 weeks, equivalent to ethanol > 80g / d, but should pay attention to gender, genetic susceptibility The influence of other factors. Ethanol amount (g) conversion formula = alcohol consumption (m1) X ethanol content (%) × 0.8. The clinical symptoms are non-specific, can be asymptomatic, or have pain in the right upper quadrant, loss of appetite, fatigue, weight loss, and the like. Alcoholism is the most important measure for the treatment of alcoholic fatty liver. During the process of alcohol withdrawal, attention should be paid to the prevention and treatment of withdrawal syndrome. If serum ALT, AST or GGT is slightly elevated, drug therapy may be considered. S-adenosylmethionine treatment can improve clinical symptoms and biochemical indicators in patients with alcoholic fatty liver disease. Polyene phosphatidylcholine has a tendency to prevent histological deterioration in patients with alcoholic fatty liver disease. Glycyrrhizic acid preparations, silymarins, polyene phosphatidylcholines and reduced glutathione have different degrees of anti-oxidation, anti-inflammatory, protection of liver cell membrane and organelles, and clinical application can improve liver biochemical indicators. basic knowledge Sickness ratio: 1-3% Susceptible people: long-term drinkers Mode of infection: non-infectious Complications: hepatic encephalopathy upper gastrointestinal bleeding liver and kidney syndrome hepatopulmonary syndrome peritonitis
Cause
Alcoholic fatty 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. 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.
Racial, genetic, and individual differences are also important risk factors for alcoholic liver disease. 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. 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.
Prevention
Alcoholic fatty liver prevention
The most effective preventive measure for alcoholic fatty liver is to abstain from alcohol, or to control the amount of alcohol consumed, and try to drink low-alcohol or non-alcoholic beverages. Do not rely too much on the preventive health products on the market today, because the brands of health care products are numerous, the treatment mechanism is unclear, and the efficacy is difficult to determine.
If you are not satisfied with the entertainment, you should avoid drinking alcohol on an empty stomach. You can take some milk or yogurt before drinking, which can protect the gastric mucosa and reduce the absorption of alcohol. Avoid using alcohol to induce vomiting, to prevent aspiration into the lungs, and acute bleeding from the tears in the stomach and esophagus.
Complication
Alcoholic fatty liver complications Complications Hepatic encephalopathy Upper gastrointestinal bleeding Hepatorenal syndrome Hepatopulmonary syndrome Peritonitis
In addition to liver damage, alcoholic hepatitis can easily cause some complications:
1. Hepatic encephalopathy: It is the most serious complication of this disease and the most common cause of death.
2, upper gastrointestinal bleeding: esophageal varices bleeding more common, often cause hemorrhagic shock or induce hepatic encephalopathy.
3, liver and kidney syndrome: manifested as oliguria or no urine, azotemia, hyponatremia and low urinary sodium.
4, alcoholic ketoacidosis: related to drinking and malnutrition, manifested as nausea, vomiting, dehydration, hyperventilation, fruity breath, acetone, acetone, hyperglycemia.
5, Zieve syndrome: triad manifestations of jaundice, hyperlipidemia and hemolysis, 40-year-old men more common, mostly after acute drinking, manifested as loss of appetite, nausea, vomiting, diarrhea, severe abdominal pain.
6, portal hypertension: can be caused by a large amount of fat deposition pressure liver sinus and hepatic vein.
7, hepatopulmonary syndrome: manifested as melena, cyanosis, clubbing, hypoxemia.
8, infection: spontaneous bacterial peritonitis is common, skin, respiratory, digestive tract and urinary tract infections can also occur.
Symptom
Alcoholic fatty liver symptoms Common symptoms Hepatic steatosis Hepatic cells have excessive accumulation of fat in the right upper quadrant Pain beer abdomen Appetite loss Weight loss
Alcoholic fatty liver disease is a liver disease caused by long-term heavy drinking. It is a type of alcoholic liver disease. Have a long history of drinking, generally more than 5 years. The clinical symptoms are non-specific, can be asymptomatic, or have pain in the right upper quadrant, loss of appetite, fatigue, weight loss, and the like.
The clinical manifestations of alcoholic fatty liver are directly proportional to the extent of liver fat infiltration, and the symptoms disappear after excessive fat removal in the liver. Clinically, hepatomegaly is the most common sign, followed by liver pain and tenderness. A small number of patients may have mild jaundice, and laboratory tests are associated with obstruction of the biliary system. Severe patients may have ascites and lower extremity edema, occasionally splenomegaly. Some patients may be accompanied by vitamin deficiency, such as peripheral neuritis, glossitis, angular cheilitis, skin ecchymosis. In conclusion, alcoholic fatty liver lacks specific clinical symptoms.
Examine
Alcoholic fatty liver examination
1, plasma protein: total plasma protein changes and white globulin ratio inversion is the most common biochemical abnormality, some patients plasma protein electrophoresis showed 1, 2, globulin increased. After the recovery of fatty liver, plasma protein abnormalities recovered later than other indicators, and returned to normal after 3 to 6 months.
2. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST): the former is not obvious, AST/ALT>2 has diagnostic significance, and ALT is not sensitive because acetaldehyde causes the enzyme cofactor B6 to decrease. ALT in liver tissue was more significantly inhibited than AST activity.
3, -glutamyl transpeptidase (-GT): alcohol is more sensitive to damage to liver cell microsomes. It is a more sensitive indicator for the diagnosis of alcoholic liver disease.
4, alcohol oral load test: detection of glycoprotein, prealbumin, 2HS glycoprotein, haptoglobin changes, decreased in alcoholic fatty liver.
5, B-ultrasound: B-ultrasound diffuse fatty liver can be divided into three types:
1 Mild fatty liver: manifested as near-field echo enhancement, far-field echo attenuation is not obvious, and the intrahepatic tubular structure is visible.
2 Moderate fatty liver: the front field echo is enhanced, the back field echo is exhausted, and the tubular structure is blurred.
3 Severe fatty liver: The near-field echo is significantly enhanced, the far field is obviously attenuated, and the tubular structure is unclear and unrecognizable. Ultrasound changes in localized fatty liver are non-uniform distribution, and the sound image shows multiple strong echogenic nodules, but no mass effect, and liver biopsy is feasible if necessary.
6, CT examination: its accuracy is better than B-ultrasound, mainly showing a general or focal reduction in liver parenchyma density.
Diagnosis
Diagnosis and diagnosis of alcoholic fatty liver
1. Have 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 pain in the right upper quadrant, loss of appetite, fatigue, loss of body mass, jaundice, etc.; as the condition worsens, there may be neuropsychiatric symptoms, spider mites, liver palm and other manifestations.
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 hepatovirus infections and drugs, toxic liver damage and autoimmune liver disease.
Meet the first, second, third and fifth or the first, second, fourth and fifth items to diagnose alcoholic liver disease; only meet the first, second and fifth suspected alcoholic liver disease.
