What Is the Relationship Between Alcohol and Jaundice?

Has a long history of alcohol consumption, usually more than 5 years, equivalent to the amount of alcohol in men 40g / d, women 20 g / d, or a large amount of drinking history in 2 weeks, equivalent to the amount of alcohol> 80 g / d, but attention should be paid to gender, genetics Susceptibility and other factors. The conversion formula of the amount of ethanol (g) = the amount of alcohol consumed (m1) x the content of ethanol (%) × 0.8. The clinical symptoms are non-specific and may be asymptomatic, or may have right upper quadrant pain, loss of appetite, fatigue, weight loss, jaundice, etc .; as the condition worsens, there may be neuropsychiatric symptoms and spider moles, liver palms and other manifestations. Laboratory tests: serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transpeptidase (GGT), total bilirubin (TBil), prothrombin time ( PT), mean red blood cell volume (MCV) and glucose-deficient transferrin (CDT) and other indicators increased. Among them, AST / ALT> 2, elevated GGT and elevated MCV are the characteristics of alcoholic liver disease, and although the CDT measurement is more specific, it is not routinely performed clinically. These indexes can be significantly reduced after drinking, and usually return to normal within 4 weeks (but GGT recovery is slower), which is helpful for diagnosis. Liver B-mode or CT examinations are typical. ^[1]

Cui Yan	(Deputy Chief Physician)	Liver Disease Center, Beijing Friendship Hospital, Capital Medical University
Wang Yu	(Deputy Chief Physician)	Liver Disease Center, Beijing Friendship Hospital, Capital Medical University

Alcoholic Hepatitis is a liver disease caused by long-term heavy drinking. It usually appears as fatty liver in the early stage, which can develop into alcoholic hepatitis, liver fibrosis and cirrhosis. Its main clinical features are nausea, vomiting, jaundice, liver enlargement and tenderness. Can be complicated by liver failure and upper gastrointestinal bleeding. Severe alcoholism can induce extensive hepatocyte necrosis and even liver failure. Alcoholic liver disease is one of the common liver diseases in China, which seriously harms people's health. In recent years, the proportion of alcoholic liver disease in hospitalized patients with liver disease has continued to rise, from 4.2% in 1991 to 21.3% in 1996; the etiology of alcoholic cirrhosis in liver cirrhosis was 10.8 in 1999 % Rose to 24.0% in 2003.

Western Medicine Name

Alcoholic liver disease

English name

Alcoholic Hepatitis

Affiliated Department

Internal Medicine-Gastroenterology

Disease site

liver

The main symptoms

Nausea, vomiting, jaundice, etc.

Main cause

Long-term heavy drinking

Multiple groups

Have a long history of drinking

Contagious

Non-contagious

Introduction to Alcoholic Liver Diseases

Has a long history of alcohol consumption, usually more than 5 years, equivalent to the amount of alcohol in men 40g / d, women 20 g / d, or a large amount of drinking history in 2 weeks, equivalent to the amount of alcohol> 80 g / d, but attention should be paid to gender, genetics Susceptibility and other factors. The conversion formula of the amount of ethanol (g) = the amount of alcohol consumed (m1) x the content of ethanol (%) × 0.8. The clinical symptoms are non-specific and may be asymptomatic, or may have right upper quadrant pain, loss of appetite, fatigue, weight loss, jaundice, etc .; as the condition worsens, there may be neuropsychiatric symptoms and spider moles, liver palms and other manifestations. Laboratory tests: serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transpeptidase (GGT), total bilirubin (TBil), prothrombin time ( PT), mean red blood cell volume (MCV) and glucose-deficient transferrin (CDT) and other indicators increased. Among them, AST / ALT> 2, elevated GGT and elevated MCV are the characteristics of alcoholic liver disease, and although the CDT measurement is more specific, it is not routinely performed clinically. These indexes can be significantly reduced after drinking, and usually return to normal within 4 weeks (but GGT recovery is slower), which is helpful for diagnosis. Liver B-mode or CT examinations are typical. ^[1]

Causes of alcoholic liver disease

There are many factors that affect the progression or exacerbation of alcoholic liver injury. At present, the risk factors that have been found in domestic and foreign studies include: alcohol consumption, drinking years, alcoholic beverage types, 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 drinking or drinking years, will greatly increase the risk of liver damage. However, due to individual differences, studies have shown that the dose-response relationship between alcohol consumption and liver damage is not very clear. There are many types of alcoholic beverages, and the damage to liver caused by different alcoholic beverages is also different. Drinking style is also a risk factor for alcoholic liver damage. Drinking on an empty stomach is more likely to cause liver damage than drinking with food. Women are more sensitive to alcohol-mediated liver toxicity, and heavier alcoholic liver disease may occur with smaller doses and shorter drinking periods than men. Consumption of the same amount of alcoholic beverages showed significant differences in blood alcohol levels between men and women.

Race, genetics, and individual differences are also important risk factors for alcoholic liver disease. The allele frequencies and genotype distributions of alcohol susceptibility genes alcohol dehydrogenase (ADH) 2, ADH3, and acetaldehyde dehydrogenase (ALDH) 2 in the Han population are different from those in Western countries, and may be Chinese alcoholics One of the reasons that the incidence of alcoholic liver disease is lower than in western countries. Alcoholic liver disease does not occur in all drinkers, but it occurs in a small group of people, indicating that there are individual differences among groups in the same area. Increasing mortality from alcoholic liver disease is related to the degree of malnutrition. Lack of vitamin A or decreased levels of vitamin E may also increase liver damage. A diet rich in polyunsaturated fatty acids can promote the progression of alcoholic liver disease, and saturated fatty acids have a protective effect on alcoholic liver disease. Obesity or overweight can increase the risk of progression of alcoholic liver disease. Hepatitis virus infection and alcohol have a synergistic effect on liver damage. Drinking alcohol on the basis of hepatitis virus infection or HBV or HCV infection on the basis of alcoholic liver disease can accelerate the occurrence and development of liver disease. ^[2]

Pathogenesis of alcoholic liver disease

ALD is mainly an inflammatory response directly or indirectly induced during the metabolism of ethanol and its derivatives. Oxidative stress, enterotoxin, inflammatory mediators, and nutritional imbalances (especially protein-caloric malnutrition) and other factors interact with each other. The result of the action. In particular, intestinal endotoxemia and endotoxin-activated Kupffer cells caused by impaired intestinal barrier function play an important role in the occurrence and development of ALD. Gut-derived endotoxin is combined with lipopolysaccharide binding protein, soluble CDl4 and other plasma proteins, and then combined with lipopolysaccharide to form a lipopolysaccharide-lipopolysaccharide binding protein complex. Lipopolysaccharide significantly increases the transcription and release of inflammatory cytokines (such as tumor necrosis factor Ct). The inflammatory factors produce amplified inflammatory effects, stimulate the transformation of stellate cells to fibroblasts, and lead to liver fibrosis. In addition, acetaldehyde adducts formed with a variety of proteins are highly immunogenic, stimulating the body to produce antibodies and causing immune damage, leading to damage to important proteins including proteases and DNA.

"Second blow" theory: As the first blow, the alcohol factor promotes the increase of reactive oxides through oxidative stress and induces liver fat accumulation. Under the action of oxidative stress-related lipid peroxidation and inflammatory cytokines, fatty liver cells undergo a second blow, causing inflammation, necrosis and fibrosis. ^[3]

Clinical manifestations of alcoholic liver disease

The clinical symptoms are non-specific and may be asymptomatic, or may have right upper quadrant pain, loss of appetite, fatigue, weight loss, jaundice, etc .; as the condition worsens, there may be neuropsychiatric symptoms and spider moles, liver palms and other manifestations.

Diagnosis and identification of alcoholic liver disease

Clinical diagnostic criteria for alcoholic liver disease:

1. Has a long history of alcohol consumption, usually more than 5 years, equivalent to ethanol 40 g / d in men and 20 g / d in women, or a large amount of alcohol consumption in the past 2 weeks, equivalent to> 80 g / dt. However, attention should be paid to the influence of factors such as gender and genetic susceptibility. The conversion formula of the amount of ethanol (g) = the amount of alcohol consumed (m1) x the content of ethanol (%) × 0.8.

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

3 Serum aspartate aminotransferase (AST), alanine aminotransferase (AL.T), gamma-glutamyl transpeptidase (GGT), total bilirubin (TBil), prothrombin time (PT ), Mean red blood cell volume (MCV) and glucose-deficient transferrin (CDT) and other indicators increased. Among them, AST / ALT> 2, elevated GGT and elevated MCV are the characteristics of alcoholic liver disease, and although the CDT measurement is more specific, it is not routinely performed clinically. These indexes can be significantly reduced after drinking, and usually return to normal within 4 weeks (but GGT recovery is slower), which is helpful for diagnosis.

4 Liver B-mode or CT examinations are typical.

5. Exclude existing infections of hepatotropic virus and drugs, toxic liver injury and autoimmune liver disease.

Diagnosing alcoholic liver disease by meeting items 1, 2, 3, and 5 or 1, 2, 4, and 5; only suspecting alcoholic liver disease by items 1, 2, and 5.

Those who meet the clinical diagnostic criteria for alcoholic liver disease are diagnosed as follows.

1. Mild alcoholic liver disease: liver biochemical indicators. Imaging and histopathological examinations were basically normal or slightly abnormal.

2. Alcoholic fatty liver: The imaging diagnosis meets the criteria for fatty liver. Serum ALT, AST, or GGT may be slightly abnormal.

3 Alcoholic hepatitis: a group of clinicopathological syndromes caused by massive necrosis of liver cells in the short term, which can occur on the basis of the presence or absence of liver cirrhosis, which is mainly manifested by increased serum ALT, AST and significantly increased serum TBil, which may be accompanied Fever, elevated neutrophils in peripheral blood. Severe alcoholic hepatitis refers to the manifestation of liver failure in patients with alcoholic hepatitis, such as coagulopathy, jaundice, hepatic encephalopathy, acute renal failure, upper gastrointestinal bleeding, etc., often accompanied by endotoxemia.

4 Alcoholic cirrhosis: clinical manifestations of cirrhosis and changes in serum biochemical indicators.

Alcoholic liver disease treatment

The treatment principles for treating alcoholic liver disease are: abstain from alcohol and nutritional support, reduce the severity of alcoholic liver disease, improve existing secondary malnutrition and symptomatic treatment of alcoholic cirrhosis and its complications.

Alcoholic liver disease

Smoking cessation is the most important measure for the treatment of alcoholic liver disease. Attention should be paid to the prevention and treatment of withdrawal syndrome during alcohol cessation.

Alcoholic liver disease nutrition support

Patients with alcoholic liver disease need good nutritional support. They should provide a high-protein, low-fat diet on the basis of abstaining from alcohol, and pay attention to vitamin B, vitamin C, vitamin K and folic acid.

Alcoholic liver disease medication

(1) Glucocorticoids can improve severe alcoholic hepatitis.

(2) Metadoxine can accelerate the elimination of alcohol from the serum and help improve symptoms and behavioral disorders of alcoholism.

(3) S-adenosylmethionine treatment can improve the clinical symptoms and biochemical indicators of patients with alcoholic liver disease. Polyene phosphatidylcholine has a tendency to prevent histological deterioration in patients with alcoholic liver disease. Glycyrrhizic acid preparations, silymarins, polyene phosphatidylcholines, and reduced glutathione and other drugs have different degrees of anti-oxidation, anti-inflammatory, protection of liver cell membranes and organelles, and clinical applications can improve liver biochemical indicators.

(4) The liver of patients with alcoholic liver disease is often accompanied by pathological changes of liver fibrosis, so anti-fibrotic therapy should be paid attention to. At present, there are a variety of traditional Chinese medicines or prescriptions for liver fibrosis.

(5) Actively deal with complications of alcoholic cirrhosis such as venous hypertension, esophageal and gastric varices, spontaneous bacterial peritonitis, hepatic encephalopathy and hepatocellular carcinoma.

(6) Patients with severe alcoholic cirrhosis can consider liver transplantation, but they are required to quit drinking for 3 to 6 months before liver transplantation, and there is no serious sperm damage of other organs. ^[4-5]

Prognosis of alcoholic liver disease

The prognostic assessment method is mainly for alcoholic hepatitis. The main recommended evaluation method is Maddrey discriminant function (MDF), MDF = 4.6 x (patient's prothrombin time-control prothrombin time) + total bilirubin (mg / d1). Patients with MDF scores 32 are at high risk of death, with a mortality rate of 30% to 50% within one month, especially those with hepatic encephalopathy will be at the highest risk. This is a dynamic mold for assessing the prognosis of patients, and its experimental results will change over time, including changes in bilirubin in the first week after admission, which is significantly related to the prognosis of patients with AH treated with prednisone.

Prevention of alcoholic liver disease

The most effective preventive measures for alcoholic liver disease are quitting alcohol, or controlling the amount of alcohol consumed, and drinking as low as possible or non-alcoholic beverages. Do not rely too much on preventive health products currently on the market, because there are many brands of health products, the treatment mechanism is unclear, and the efficacy is difficult to determine.

If there is entertainment that is not easy to shirk, to avoid drinking on an empty stomach, you can take some milk, yogurt, etc. before drinking, which can protect the gastric mucosa and reduce alcohol absorption. Do not use drunk vomiting to prevent aspiration into the lungs and acute bleeding caused by tears in the stomach and esophagus.

Alcoholic liver disease diet note

Patients with alcoholic liver disease need good nutritional support. They should provide a high-protein, low-fat diet on the basis of abstaining from alcohol, and pay attention to vitamin B, vitamin C, vitamin K and folic acid.