Alcoholic hepatitis

Introduction to alcoholic hepatitis Alcoholic Hepatitis refers to a liver disease caused by prolonged excessive drinking. Its main clinical features are nausea and vomiting, jaundice, liver enlargement and tenderness. Can be complicated by liver failure and upper gastrointestinal bleeding. The typical age of onset is concentrated between 40 and 60 years old. More men than women. A study of 1,604 cases of alcoholic patients undergoing liver biopsy (liver wear) biopsy has a prevalence of approximately 20%. Alcoholic hepatitis is also a clinical classification of alcoholic liver disease. It is a group of clinical pathological syndromes caused by massive necrosis of hepatocytes in a short period of time. It can occur on the basis of with or without cirrhosis, mainly due to elevated serum ALT and AST. And serum total bilirubin is significantly increased, may be associated with fever, peripheral blood neutrophils. Severe alcoholic hepatitis is a manifestation of liver failure in patients with alcoholic hepatitis. Such as coagulation mechanism disorders, jaundice, hepatic encephalopathy, acute renal failure, upper gastrointestinal bleeding, etc., often accompanied by endotoxemia. basic knowledge The proportion of the disease: the incidence of this disease in the alcoholic population is about 0.01%-0.02% Susceptible people: between 40-60 years old Mode of infection: non-infectious Complications: jaundice, hepatic encephalopathy

Cause of alcoholic hepatitis

Drinking alcohol is the main cause of alcoholic hepatitis.

Etiology

The incidence of alcoholic hepatitis and the severity of liver damage are linearly positively correlated with the length of alcohol abuse and the dose. In Europe and the United States, the incidence rate is significantly higher than that of China, and severe alcoholic liver damage has an increasing trend among women. About 10% to 20% of alcoholics have different degrees of alcoholic liver disease. More than 90% of ethanol is oxidatively metabolized in the liver to form acetaldehyde and acetic acid. Ethanol can be reduced to NADH during the oxidation of alcohol dehydrogenase and microsomal enzymes, and when acetaldehyde is oxidized to acetate or acetyl-CoA, causing the intracellular environment to be reduced, thereby interfering with sugar and lipids. Class and some intermediate metabolic links. Decreased gluconeogenesis, increased synthesis of fatty acids and triglycerides, reduction of oxaloacetate to malate, and decreased carboxyreactivity may cause hypoglycemia, hypertriglyceridemia, accumulation of intrahepatic fat and interference with energy metabolism. The reduction of pyruvate to lactic acid promotes the development of hyperuricemia and acidosis. Ethanol and acetaldehyde have a direct toxic effect on the liver. Long-term alcohol abuse can increase the hepatotoxic effects of commonly used drugs, certain vitamins, hepatotoxic substances in the environment and carcinogens.

Pathological change

Alcoholic liver disease is a trilogy in pathology: fatty liver alcoholic hepatitis cirrhosis, and the three often overlap. The histological features of alcoholic hepatitis are acute or chronic hepatic inflammatory lesions, including hepatocyte vacuolar degeneration, necrosis, ethanolic transparent bodies (Mallory bodies), neutrophil neutrophils and lymphocytic infiltration, fibrous tissue Hyperplasia and cholestasis. Peripheral hepatic venous fibrosis or sclerosing glassy necrosis can occur in portal hypertension before cirrhosis. Mallory is a specific lesion of alcoholic biliary disease, but it is also found in some primary biliary cirrhosis, Wilson's disease, pediatric cirrhosis in India, cirrhosis after liver bypass and hepatocellular carcinoma Wait. The corpuscle is caused by fibrin deposition in the cytoplasm, which is characterized by high-density eosinophils of different shapes and sizes in the vicinity of hepatocytes, which may contain a small amount of fat. Mallory bodies are 2 to 3 m in diameter and are filamentous, irregularly surrounded or horseshoe-shaped around the hepatocyte nucleus. Under the electron microscope, the small body is composed of numerous irregular intermediate fibers.

Alcoholic hepatitis prevention

The most effective preventive measure for alcoholic hepatitis is to stop drinking, 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.

Alcoholic hepatitis complications Complications, jaundice, hepatic encephalopathy

Can be complicated by jaundice, hepatic encephalopathy, acute renal failure and so on.

Alcoholic hepatitis symptoms Common symptoms Ascites liver ascites fever jaundice severe jaundice liver qi spleen liver qi stagnation of stomach and liver capsules

Because alcoholic hepatitis is a histopathological diagnosis, the clinical manifestations vary in severity, can be asymptomatic, or jaundice, and can also die from complications. Often developed from fat, it can also overlap with cirrhosis.

Symptom

Patients often have a history of heavy drinking in the near future, which may have loss of appetite, nausea, vomiting, abdominal pain and weight loss, and may have fever. The severity of symptoms is often consistent with the degree of histological changes in the liver, but some patients may have no symptoms. There were 89 cases of patients with alcoholic hepatitis confirmed by liver biopsy, serum total bilirubin 85.5 mol / L, 51% of patients without liver-related symptoms.

2. Signs

The disease is characterized by jaundice, liver enlargement and tenderness. 80% to 100% of patients have hepatomegaly. 10% to 70% manifested as ascites, fever, splenomegaly, spider mites and neuropsychiatric symptoms. In some patients, the bilateral parotid glands were moderately enlarged.

Alcoholic hepatitis often has a history of heavy drinking in the near future, with obvious abdominal distension, general fatigue, loss of appetite, diarrhea, nausea and vomiting, abdominal pain, weight loss, fever in some patients, and leukocytosis (mainly neutral). Granulocyte enlargement), like a bacterial infection. Lischner analyzed 169 cases of alcoholic hepatitis with 77% loss of appetite, 55% of nausea and vomiting, 46% of abdominal pain, and 43% of weight loss.

In alcoholic hepatitis cases, the number of drinking years is 8.5 to 41 years, with an average of 21 years. The amount of alcohol consumed is 60-200g/d, with an average of 117g/d. According to the aforementioned pathological classification of 24 cases, 15 cases were mild, 6 cases were moderate, and 3 cases were severe. There was no statistically significant difference in the average drinking time and average alcohol consumption.

It is characterized by jaundice, hepatomegaly and tenderness. A few have splenomegaly, dull complexion, ascites, edema, and spider mites. When there is liver dysfunction, the ascites is obvious, and some have neuropsychiatric symptoms. Among the 169 cases reported by Lischner, hepatomegaly 81%, jaundice 77%, ascites 59%, fever 56%, malnutrition 55%, upper gastrointestinal bleeding 22%, esophageal varices 12%, and mental symptoms 10%. Among the 24 cases of Sino-Japanese Friendship Hospital, hepatic enlargement was 58%, alcoholic face was 50%, liver palm 46%, weight loss 46%, spider mites 38%, jaundice 33%, spleen enlargement 21%, ascites 12.5%, esophageal varices In 1 case, 2 cases of esophageal vein were exposed, and 1 case of fever was 38.1 degrees Celsius. The literature reports that most of the fever patients with the suspension of alcohol after hospitalization, fever also returned to normal within a few days, but individual patients can be fever for up to 4 weeks.

As for the relationship between the mild, moderate and severe pathological changes and clinical, 24 patients in this group from the laboratory examination items including ALT, AST, ALP, GGT values increased (light alcoholic hepatitis was 43%-72%; moderate 60 %-80%; severe 100% increase), and decreased prothrombin activity. Clinical signs: fatigue, liver pain, sexual dysfunction, impotence, hepatomegaly (36%-71% hepatomegaly in mild alcoholic hepatitis, moderate 2/3 hepatomegaly, severe hepatomegaly) For reference.

These examination items are all non-specific for alcoholic hepatitis. Therefore, it is not clear whether to distinguish between mild, moderate and severe in the specific patients. It is not necessary to distinguish between mild, moderate and severe. To help determine the severity.

Alcoholic hepatitis check

Hematological examination

There may be anemia, leukocytosis, and abnormal red blood cells, such as target, thorn, mouth, and giant red blood cells, with an increase in mean red blood cell volume (MCV).

2. Biochemical examination

Serum bilirubin increased, aspartate aminotransferase (AST) activity increased significantly, while alanine aminotransferase (ALT) activity only slightly increased or normal. Therefore, the ratio of AST:ALT increases. If the ratio is >2, the sensitivity for the diagnosis of alcoholic liver disease is 68%, the specificity is 91%, and the positive predictive value is 82%. Alkaline phosphate and r-glutamyltranspeptidase (r-GT) activity is increased. r-GT is a sensitive but not specific indicator. Combined detection of MCV, rG and alkaline phosphatase is an ideal laboratory indicator for the diagnosis of alcoholic liver disease.

3. Liver B-mode ultrasound and CT examination

Helps to find fatty liver. The diagnosis depends on the liver biopsy. Because the liver damage is diffuse, a non-positioning needle biopsy is feasible.

Diagnosis and identification of alcoholic hepatitis

diagnosis

According to the patient's long history of massive alcohol abuse; clinical fever, jaundice, hepatomegaly tenderness and increased white blood cells; MCV, r-GT, alkaline phosphatase increase, AST / ALT > 2 contribute to the diagnosis of alcoholic hepatitis, but Confirmation of the diagnosis requires liver biopsy. Diagnostic errors are often caused by presumed liver histological changes based on traditional laboratory results, because changes in enzymes, such as alcoholic liver disease, are extremely poorly correlated with histopathology. It has been reported that 89 patients with liver perfusion confirmed alcoholic hepatitis, 49% of serum bilirubin was normal, 19% of AST was normal, 37% of alkaline phosphatase was not elevated, and 59% had normal levels of serum albumin. However, 38% of cirrhosis occurred after 30 months, and the mortality rate was 22%.

Differential diagnosis

The differential diagnosis should be clear whether it is chronic alcoholism or alcoholic liver disease; which stage of alcoholic liver disease belongs to it; and it is differentiated from other liver diseases. Among them, blood alcohol concentration and liver biopsy are the most important differential diagnosis methods. The disease should be differentiated from liver abscess, biliary disease, metastatic liver cancer and sepsis.

Staging of alcoholic hepatitis

First, mild alcoholic liver disease

The patient's clinical symptoms are mild, liver function is normal or mild abnormality. The diagnosis depends mainly on the detailed history of drinking, combined with clinical and liver biopsy to help diagnose. This type accounted for 31.3% of 136 cases of alcoholic liver disease in China-Japan Friendship Hospital, which was larger than that reported in Japan.

Mild alcoholic liver disease can be seen in the basic pathological changes of alcoholic liver disease, such as large bubble lipid changes, strong balloon-like changes, necrosis with PMN infiltration and lobular fibrosis in the center of the lobule, but the degree of lesions is light, both at level 1 range. Due to the mild lesions, the structure of the hepatic lobule is not destroyed, and it can be completely recovered after abstinence.

Second, alcoholic fatty liver

The clinical symptoms are more mild, and there are different degrees of hepatomegaly. The liver weight often reaches 2000-2500g, even more than 3000g (normal 1200-1500g). The liver is yellow in color and has a blunt edge. In most patients, the lipids of the patients become macrovesicular lipids, which are mainly found in the distribution of the 2,3 regions of the liver acinus, and the diffuse distribution is severe.

Third, alcoholic hepatitis

Alcoholic hepatitis occurs in chronic alcoholics and often has a history of continued heavy drinking in the short term. Alcoholic hepatitis can be asymptomatic but usually associated with non-specific gastrointestinal symptoms, hepatomegaly, elevated liver enzymes, 25% severe liver damage, patients may have fever, anorexia, jaundice, elevated white blood cells, liver failure may also occur Or hepatic encephalopathy.

Fourth, alcoholic liver fibrosis

Various types of chronic alcoholic liver disease are associated with different degrees of liver fibrosis. Alcoholic liver fibrosis is an independent type that has been adopted by some scholars in the past decade.

Alcoholic hepatitis The basic lesions of alcoholic liver fibrosis include: sinus fibrosis, terminal venous fibrosis, fibrosis around the portal area and portal area, and bridging fibrosis (interval formation). Alcoholic liver fibrosis is classified into light, moderate, and severe depending on the extent and extent of fibrosis. Lipids and inflammation can be associated with all types, but the degree of both is lighter than the degree of fibrosis.

Mild alcoholic liver fibrosis is characterized by pronounced periorbital fibrosis with a few fibrous septa formation, but the lobular structure remains. Moderate alcoholic liver fibrosis has a wide range or moderate to severe sinusoidal fibrosis, fibrous interstitial, resulting in lobular structural disorders, some patients may have signs of portal hypertension, including esophageal varices, splenomegaly and ascites, continue Developed into severe alcoholic liver fibrosis, early cirrhosis.

Five, alcoholic cirrhosis

Alcoholic cirrhosis is characterized by small nodular cirrhosis and enlarged liver. Early alcoholic cirrhosis nodules are very small, the characteristics of the microscope are small hepatocyte nodules, no regeneration, and more in the portal area. Fibrosis from the end of the hepatic vein, along the 3 area and the portal area, forming a wide gap of vascular fibers containing dilated sinusoids, often along the 3 area to divide the lobular acinus into tiny nodules.

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