What Is Acute Hepatitis?

Acute hepatitis is a collective term for a class of diseases. Although the etiology is different, its clinical characteristics, treatment methods, and prognostic outcomes have many common characteristics: liver function presents obvious acute damage, and ALT increases more than 10 times, that is,> 400 U / L , Usually it can reach 1000-2000 u / l, which can be accompanied by jaundice; liver tissues have varying degrees of necrosis, no fibrous connective tissue hyperplasia, and disease development can be smoothly recovered. The acute phase requires rest and active liver protection treatment.

Wang Xiaomei	(Chief physician)	Liver Disease Center of Beijing Ditan Hospital
Xing Huichun	(Chief physician)	Liver Disease Center of Beijing Ditan Hospital
Cheng Danying	(Attending physician)	Liver Disease Center of Beijing Ditan Hospital

Acute Hepatitis: refers to a variety of pathogenic factors that invade the liver, causing damage to liver cells, impaired liver function, and then cause a series of uncomfortable symptoms in the human body. The course of these damages does not exceed six months. These common pathogenic factors are viruses, bacteria, parasites, chemical poisons, drugs and poisons, alcohol and so on. In China, the most common acute hepatitis is acute viral hepatitis, especially acute hepatitis B. Abroad, most are alcoholic hepatitis. It should be noted that usually the acute hepatitis in our lives refers to acute viral hepatitis, which is only a branch of "acute hepatitis". The acute hepatitis mentioned above refers to the concept in a broad sense. It is not limited to viral hepatitis.

Western Medicine Name: Acute hepatitis
English name: Acute Hepatitis
Affiliated Department: Internal Medicine-Gastroenterology
Disease site: liver

The main symptoms: Low fever, general fatigue, loss of appetite, nausea, vomiting, etc.
Main cause: Viruses, bacteria, parasites, chemical poisons, drugs and poisons, alcohol, etc.

Introduction to Acute Hepatitis

Causes and classification of acute hepatitis

Classification according to cause

1. Acute viral hepatitis: At present, there are five types of hepatitis viruses that can cause disease: A, B, C, D, and E. The relationship between other candidate viruses and liver diseases, especially fulminant liver failure and chronic hepatitis, has not been widely recognized.

Viral hepatitis is one of the most widely spread infectious diseases in the world. As early as 400 BC, Hippocrates described epidemic jaundice, and it was not until the 8th century AD that Pope Zacharias observed the infectious properties of the disease. It was only in 1908 that the virus was also found to be one of the causative factors of hepatitis. In 1947, the original infectious hepatitis was called Hepatitis A (HA); serum hepatitis was called Hepatitis B (HB). The surface antigen of hepatitis B was first detected in humans in 1965.

In addition, viral hepatitis includes hepatitis C, hepatitis D, hepatitis E, and hepatitis G. A virus that was previously identified as Hepatitis B virus is now identified as a genus of Hepatitis B virus, so Hepatitis B does not exist.

2. Alcoholic hepatitis: Alcoholic hepatitis may have no obvious symptoms in the early stage, but the liver has pathological changes. Excessive alcohol consumption (equivalent to 80 g / d of alcohol) within 2 weeks can cause the manifestation of acute hepatitis with significant weight loss, loss of appetite, nausea, vomiting, general malaise, fatigue, fever, abdominal pain and diarrhea, upper gastrointestinal bleeding and mental symptom. Signs are jaundice, hepatomegaly, and tenderness.

3. Drug-induced hepatitis: Many drugs can cause hepatitis. For example, in 2000, the United States withdrew its license for treglitazone, a diabetes treatment drug, which caused hepatitis. Other hepatitis-related drugs are: trifluorobromochloroethane, methyldopa, isoniazid, rifampicin and pyrazinamide, phenytoin zinc and valproic acid, zidovudine, ketoconazole, nifedipine , Ibuprofen and indomethacin, amitriptyline, amiodarone, furantoin, oral contraceptives, choline alcohol, azathioprine. Some Chinese herbs and food supplements can also cause hepatitis.

Different drugs and patients' response to drugs can make the development of drug-induced hepatitis very different. For example, trifluorobromochlorohepatitis caused by ethane and isoniazid can be very mild, but it can also be fatal.

Depending on each person's situation, virtually any drug can cause hepatitis in some people.

Other poisons also cause hepatitis. Poisonous mushrooms, yellow phosphorus, etc.

Excessive acetaminophen can cause hepatitis, and taking acetylcysteine in time can reduce the damage to the liver. Carbon tetrachloride, chloroform, acetylene trichloride, and all other organochlorines can cause steatohepatitis.

4. Infectious toxic hepatitis: secondary to toxic liver lesions following bacterial infection. Severe infections such as sepsis, typhoid fever, and fulminant meningoencephalitis can cause toxic hepatitis. Younger infants are more common, and most of them have obvious pre- or concurrent infections.

According to the presence or absence of jaundice in patients, acute hepatitis can be divided into two types: acute jaundice hepatitis and acute jaundice-free hepatitis:

Acute jaundice hepatitis

Acute onset, rapid development of the disease, yellow skin and eyeballs of varying degrees. The course of disease is about 2-3 months, with hepatitis A and E being more common.

2. Acute non-jaundice hepatitis

This type is more common than jaundice, with hepatitis B being the majority, and some being hepatitis C. Most are slowly onset.

The most prominent manifestations are symptoms of loss of appetite, general weakness, and pain in the liver. Some patients have nausea and vomiting, dizziness and headache, and may have fever and upper respiratory symptoms. Most cases have hepatomegaly with tenderness and throbbing pain. Liver damage is not as significant as the jaundice type. Most returned to health within 3-6 months, but some cases became prolonged and became chronic.

Pathological changes in acute hepatitis

The pathological changes of acute hepatitis are: macroscopic view, hepatomegaly, soft texture, and smooth surface.

It can be seen under light microscopy that hepatocytes have extensive degeneration and are mainly cell edema, which is manifested by hepatocellular cytoplasmic loose staining and balloon-like changes. Balloon-like changes are the most common. Under the electron microscope, the endoplasmic reticulum was significantly enlarged, the ribosome was shed, the mitochondria were reduced, the ridge was broken, and the glycogen decreased and disappeared. Highly balloon-like degeneration can develop into lytic necrosis. In addition, eosinophilic and coagulative necrosis of liver cells can also be seen, and organelle aggregation under electron microscope. ^[1]

Pathogenesis of acute hepatitis

After being infected with hepatitis A virus, it only causes slight damage to the liver and thorax during the process of intrahepatic replication. After a series of immune responses (including cellular immunity and humoral immunity) occur in the body, the liver has obvious lesions and appears as liver cells. Necrosis and inflammatory response. Hepatitis A virus HAV is cleared by the body's immune response, so it generally does not develop into chronic hepatitis, cirrhosis or viral carrier.

Hepatitis B virus infects and replicates in hepatocytes, and it is generally believed that hepatocyte disease is not directly caused. However, the hepatitis B virus HBV gene will integrate into the host's hepatocyte chromosome and may have long-term effects. The liver cell damage of hepatitis B is mainly caused by a series of immune responses in the body, of which cellular immunity is the main. Specific antibodies combine with the corresponding antigens and virus particles in the circulation to form immune complexes, which are cleared by phagocytic cells. Certain circulating immune complexes can be deposited on the basement membrane of small blood vessels, in the joint cavity and on the small blood vessel walls of various organs, causing rash, arthritis, glomerulonephritis, nodular multiple arteritis and other extrahepatic diseases . Infected liver cells are killed, and hepatitis B virus is eliminated by protective antibodies (anti-HBs, especially anti-pre-S2), which can lead to termination of the infection.

The pathogenesis of hepatitis C remains unclear. Studies have shown that HCV causes viremia after entering the body. The concentration of HCV in plasma is about 100-100000000 / ml. Viremia occurs intermittently throughout the course of the disease. HCV RNA can be detected from blood or liver tissue by PCR in the first week. Beginning in the second week, anti-HCV can be detected. Anti-HCV was detected in a small number of cases after 3 months of infection. Due to the lack of an appropriate cell culture system, research on the pathogenesis of HCV is limited. Current research suggests that HCV-induced liver cell damage involves the direct killing effect of HCV HCV, host's own immunity, and apoptosis. Among them, the immune response plays a more important role. Therefore, HCV-infected patients are often accompanied by autoimmune changes. For example, bile duct pathological damage is similar to autoimmune hepatitis; autoimmune diseases are often combined, and a variety of autoantibodies can be detected in the serum.

In addition, HCV infection tends to become chronic, and more than 80% of HCV infected patients become chronic.

Animal experiments on hepatitis D have shown that HDV and HBV overlap infection lead to a large number of HDV replication, which is significantly more than those with HDV and HBV combined infection. HDV is directly pathogenic to liver cells. Hepatitis B is accompanied by HDV infection, especially in patients with overlapping infections, and liver cell damage is significantly worsened.

Hepatitis E virus may be mainly infected orally, and then enter the liver by intestinal blood circulation. After proliferation and replication in liver cells, it is excreted into blood and bile, and finally excreted in the feces. Whether there is extrahepatic replication has not been concluded yet. It has also been shown that liver lesions are primarily virus-induced cellular immune responses that mediate hepatocyte lysis.

There is no cross-immunity between all types of viral hepatitis. HDV and HBV combined infection or overlapping infections can aggravate the disease and easily develop into chronic hepatitis and severe hepatitis, especially those with HDV overlapping infection in chronic hepatitis B. HAV or HBV overlap infection also exacerbates the condition and can even progress to severe hepatitis.

Alcoholic hepatitis pathogenesis: Alcohol causes damage through a variety of mechanisms, roughly divided into two independent but related pathways, including direct damage to liver cells by alcohol and activation of endotoxins and cytokines, immune-mediated mechanisms, Indirect damage caused by fibrogenesis. Superimposed on these hepatocellular mechanisms is that alcohol intake impairs liver regeneration.

Drug-induced hepatitis: due to the toxic effects of drugs and their metabolites or the body's allergic reactions to drugs, causing damage to the liver and causing liver inflammation. details as follows:

The direct damage of drugs to liver cells reduces liver blood flow, decreases the detoxification function, decreases drug clearance, and promotes drug accumulation. Highly toxic drugs can directly damage the entire liver cells and cause hepatocyte necrosis. Indirect poisons with low toxicity can Selective damage to the bile excretion system.

As a hapten, the drug can interact with carrier proteins in the liver and cause drug allergy and damage liver cells. Some people have hypersensitivity to specific drugs.

Indirect damage of drug intermediate metabolites, some liver damage is related to toxic metabolites produced during drug conversion.

Infectious toxic hepatitis: liver infections of various bacteria, fungi, and rickettsial organisms, which may directly invade hepatocytes or bile ducts, or may be caused by toxic products. In addition, the process of systemic infection often causes jaundice or non-specific liver biochemical abnormalities, and the mechanism is not yet clear. ^[2-3]

Clinical manifestations of acute hepatitis

Early symptoms after acute hepatitis infection: The patient recently developed low fever, general fatigue, and loss of appetite, accompanied by nausea, vomiting, greasiness, discomfort in the liver area, and yellow urine. He did not improve after rest.

General classification symptoms:

1. Acute jaundice hepatitis

(1) Pre-jaundice: Onset is slow, joint fever and rash often appear with mild or no fever. Common symptoms are fatigue, loss of appetite, greasiness, nausea, vomiting, and sometimes abdominal pain and diarrhea. This period lasts an average of 5-7 days.

(2) Jaundice: fever subsides, conscious symptoms ease slightly, and jaundice appears on the sclera and skin, reaching a peak within a few days to 3 weeks. Dark yellow urine may appear transient lightening of stool. Pain in the liver area, large liver, soft texture, tenderness and tenderness. This period lasts 2-6 days.

(3) Recovery period: The patient's jaundice gradually reduced and subsided, the stool color returned to normal, skin itching disappeared, appetite improved, physical strength recovered, gastrointestinal symptoms decreased, jaundice resolved, and liver function returned to normal. This period is generally 1-2 months.

2. Acute non-jaundice hepatitis

This type is more common, with milder symptoms, general weakness, loss of appetite, nausea, and abdominal distension. Signs are more common liver, softer, tenderness and tenderness. The diagnosis of this type of hepatitis symptoms is often overlooked. The course of disease is about 2-3 months.

Sometimes the severity of the condition is different, and the severity of the symptoms or signs is also different.

Acute severe hepatitis, also known as fulminant hepatitis. The clinical features are acute onset, with disturbances of consciousness, bleeding, jaundice, and liver shrinkage within 10 days. The course of the disease does not exceed 3 weeks. The early clinical manifestations of fulminant hepatitis are similar to acute jaundice hepatitis, but the disease progresses rapidly, so the following symptoms occur, and a severe diagnosis should be considered.

(1) Obvious symptoms of systemic poisoning. With the progressive deepening of jaundice, the patient is extremely weak, debilitated, lethargic or insomnia, personality changes, mental abnormalities, impaired computing power and disorientation, flutter-like tremor, and unconsciousness.

(2) Severe gastrointestinal symptoms, marked loss of appetite, and even anorexia, frequent nausea, vomiting, and high abdominal distension.

(3) Jaundice progresses progressively, serum total bilirubin rises to more than 171umol / L within a few days, while serum alanine aminotransferase decreases or even normal, and bile enzyme separation occurs. There are also a small number of patients whose disease progresses rapidly, and the jaundice is not obvious before the disturbance of consciousness.

(4) The liver or liver dullness progressively shrinks, and ascites appears rapidly within a few days of onset. Liver CT and B-ultrasounds revealed liver atrophy.

In the above situation, the condition is very serious, and if not actively treated, the mortality rate is extremely high. ^[4]

Acute hepatitis complications

Acute hepatitis complications are rare, but can also occur. For example, common complications of the digestive system include cholecystitis, pancreatitis, gastroenteritis, endocrine system complications include diabetes, hematological complications aplastic anemia, hemolytic anemia, and circulatory system complications include myocarditis and nodular Multiple arteritis, urinary system complications include glomerulonephritis, tubular acidosis and so on. Skin complications include allergic purpura.

Diagnosis and diagnosis of acute hepatitis

Diagnosis of Acute Hepatitis

I. Classification According to the presence or absence of jaundice, it can be divided into acute jaundice hepatitis and acute jaundice-free hepatitis.

2. Medical history There is a history of close contact with patients with viral hepatitis, a history of blood and body fluid infections, and a history of water and food contamination in the outbreak endemic area. Recent history of suspected damage to drugs or poisons. He had a large drinking history within 2 weeks.

Third, the symptoms are more acute onset. Fever, nausea, anorexia, poor appetite, abdominal distension, clear stools, and apparent weakness. Most have mild to moderate hepatomegaly, soft texture, often tenderness or throbbing pain, the spleen can be slightly enlarged, and some have jaundice.

Fourth, auxiliary inspection

(1) Disease diagnosis and examination The liver function examination showed abnormal elevation of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and / or bilirubin. Imaging studies, such as liver ultrasound, often indicate liver inflammation.

(II) Pathological examination of pathogens currently uses immunological, enzymatic and molecular biological methods for pathogen detection. Liver tissue immunohistochemistry and immunoelectron microscopy are helpful for pathogen typing.

1. Hepatitis A: serum anti-HAVIgM is positive in the acute phase. The total anti-HAV antibody titers of the serum in the acute phase and the recovery phase increased by more than 4 times. HAV particles were detected by faecal immunoelectron microscopy in the early stage. HAAg was detected in the early feces. A positive HAV infection can be diagnosed as a recent HAV infection. HAVRNA was detected in serum or stool.

2. Acute hepatitis B: A diagnosis can be made with one of the following dynamic indicators. Titer of HBsAg from high to low, anti-HBs positive after disappearance. Acute phase serum anti-HBc-IgM showed high titer, while anti-HbcIgG (a) or low titer.

3 Hepatitis C

Can be used for serum antibodies (anti-HCV), serum hepatitis C virus RNA (HCV-RNA), etc., immunohistochemical detection of liver tissue HCV antigen is a more specific method.

4 Hepatitis D: simultaneous or overlapping infection with HBV.

(1) Anti-HD-IgM positive or anti-HD positive or HDAg positive in serum.

(2) HDV RNA was positive in serum.

(3) HDAg is positive in liver tissue.

5. Hepatitis E-specific diagnosis: serum anti-HEV-IgM positive in the acute phase, or HEV particles found in the acute phase of fecal immunoelectron microscopy, or those with negative anti-HEV in the acute phase and positive conversion in the recovery phase.

Differential diagnosis of acute hepatitis

Acute jaundice hepatitis

1. Pre-jaundice: should be distinguished from upper respiratory tract infection, infectious mononucleosis, rheumatic fever and gastroenteritis.

2. Jaundice: It should be distinguished from other diseases that can cause jaundice, such as drug-induced hepatitis, leptospirosis, infectious mononucleosis, cholecystitis, and cholelithiasis.

Jaundice-free hepatitis

It should be distinguished from other diseases that can cause liver (spleen) enlargement and liver function damage, such as chronic schistosomiasis, clonorchiasis, and fatty liver.

Acute hepatitis disease treatment

The treatment of acute hepatitis is mainly supportive. Combined with the condition, pay attention to rest during the acute phase, give a reasonable diet, quit smoking and alcohol, and other comprehensive treatments such as liver and choleretic drugs, which will help recover the condition. In the early course of the disease when acute symptoms are obvious and liver damage is severe, bed rest should be given mainly, and light and easy-to-digest foods should be given, supplemented with appropriate drug treatment to control symptoms, promote liver disease recovery, and prevent the development and transformation of the disease. Chronic; When the condition is stable or after the recovery period, bed rest should be a combination of movement and static, adjust the diet to meet nutritional needs, and choose drug-assisted treatment based on the condition. Avoid alcohol, fatigue, infection with other pathogens, and the use of liver toxicity drugs. At the same time, pay attention to maintain a happy mood, build confidence, and cooperate with treatment, the vast majority of patients are expected to recover quickly. The natural course usually does not exceed 2-4 months. The difference between hepatitis C and other types of viral hepatitis is that antiviral treatment must be carried out as early as possible, so as to prevent chronicization or slow down the sexualization process. It is generally believed that the shorter the duration of hepatitis C infection, the lighter the liver tissue lesions, the lower the amount of virus in the blood, and the better the efficacy of antiviral therapy.

Prognosis of acute hepatitis disease

Hepatitis A: Chronic disease does not occur, but about 10% can be manifested as a prolonged course of disease and 3% can recur, mainly in adults. The course of the disease lasted from 3 to 6 months, and the main manifestation was that the alanine aminotransferase did not fall to normal levels, and there were no conscious symptoms. Hepatitis A recurrence mostly occurs within 3-6 months after the illness, but clinical symptoms recur, but it is milder than the previous acute disease and more jaundice-free.

Acute hepatitis B: The vast majority are self-limiting. After general symptomatic and adjuvant drug treatment, more than 90% of acute hepatitis B can be recovered without routine antiviral treatment. However, 5% to 10% of patients with acute hepatitis B have been converted to chronic hepatitis B. In part, due to the low immune function of the body, the hepatitis B virus persists in the body, and liver disease cannot be recovered for a long time. It is necessary to closely observe the clearance of the hepatitis B virus and give it if necessary. Antiviral treatment prevents the development of chronic hepatitis.

Acute hepatitis C: Approximately 80% of patients with acute hepatitis C who have not received antiviral treatment have become chronic hepatitis C, and some patients will gradually develop cirrhosis and liver cancer. The natural cure for acute hepatitis C is less than 20%, which is much lower than the acute hepatitis B infection.

Hepatitis E: The vast majority have a good prognosis. Chronic cholestasis of the elderly hepatitis E is more common and the disease is more severe, and a few develop severe hepatitis. Some patients have a prolonged disease, but do not progress to chronic hepatitis, and there is no risk of evolution to liver cancer. HBsAg-positive carriers and pregnant women with hepatitis E virus infection in the third trimester of pregnancy tend to develop severe hepatitis with a mortality rate of up to 20%.

Alcoholic hepatitis: If liver function returns to normal, it can be restored if alcohol and hospitalization can be taken in time. If patients continue to drink alcohol, they will inevitably develop cirrhosis or concurrent liver failure, and some alcoholic hepatitis will develop liver fibrosis instead of cirrhosis. According to statistics, the mortality rate is more than 50% within 7 years. Occasionally died of shock, hypoglycemia, and acute pancreatitis caused by pulmonary fat embolism.

Drug-induced hepatitis: After discontinuation of drugs that can damage the liver, the corresponding treatment is given, and the condition recovers more quickly. If he continues to take drugs for liver damage after recovery, some patients may progress to drug-induced liver cirrhosis with a poor prognosis.

Infectious Toxic Hepatitis: The prognosis of this disease is related to the degree of its infection and poisoning. Mild cases can be cured quickly after symptomatic treatment. In severe cases, the prognosis is poor.

Acute hepatitis disease prevention

Patients with acute viral hepatitis need to pay attention to isolation. Hepatitis A and E should strengthen personal hygiene and stool management. Hepatitis B, C, and D should be prevented from spreading through blood and body fluids. Vulnerable populations can be vaccinated against live hepatitis A vaccine and hepatitis B vaccine for active immunization; human serum or placental globulin can also be used to prevent hepatitis A, which can be applied after being accidentally acupunctured by a syringe containing the body fluid of a hepatitis B patient Hepatitis B immunoglobulin injection to prevent hepatitis B infection.

Acute hepatitis diet attention

As for hepatitis patients, there is a saying "three points rule and seven points support", the focus is on how to recuperate. Diet therapy is also an important means to promote the recovery of acute hepatitis. During the illness, pay attention to rest, adjust the diet structure, combine medicine and food, promote appetite, and combine with the specific circumstances of each patient. Make a practical diet plan for people, places, and times. The diet of general hepatitis patients should Fresh, digestible, and contains a certain amount of protein, carbohydrates and vitamins B and C. Nutritional treatment of patients with acute hepatitis should emphasize high protein, high carbohydrate, high vitamin, and low fat foods, that is, "three high and one low."

1. High protein: The liver is an important organ for protein breakdown and synthesis in the body. The liver has pathological changes that affect the secretion of digestive enzymes, weaken the gastrointestinal motility, hinder the digestion and absorption of food, and reduce protein absorption and synthesis. In liver disease, the protein Decomposition is accelerated, a large amount of protein is lost, and plasma protein is reduced, making it difficult to repair damaged liver tissue, and even local edema and ascites due to low protein, so a high-protein diet should be supplemented. When eating, pay attention to both the amount of protein and the quality. In high-protein foods, it is necessary to choose foods rich in amino acids, such as eggs, milk, lean meats and soy products, and fatty meats containing too much fat are not easy to digest after eating, and often have a feeling of bloating, so they are not suitable for consumption. Meat food should be fish, rabbit, chicken, lean pork and so on. Bean protein, such as soy products, and food with animal protein, have complementary effects, can improve its physiological value, but those who have indigestion and have a feeling of fullness after eating, should not eat more tofu.

2. High carbohydrates: Sugar is the body's source of calories, so pay attention to sugar supplements. However, the supply of sugars should be appropriate and should not be excessive. Too much sugar will affect the secretion of gastric acid and digestive enzymes, thus reducing appetite. Carbohydrates are easily fermented and produce a large amount of gas, which can easily lead to bloating, especially when the patient's spleen and stomach function is diminished. At the same time, the glucose metabolism process is faster than fat, thus replacing fat breakdown, leading to fat storage, easy to gain weight or producing fatty liver, which affects the treatment of hepatitis. Therefore, the supply of hepatitis dietary sugar should be appropriate and not excessive.

3. Vitamin supplementation: When the liver is damaged, vitamin intake and synthesis are reduced, and consumption is increased to cause deficiency. Therefore, it is necessary to supplement B vitamins, vitamin C, and vitamin A appropriately. Animal livers are rich in vitamin B, which is about 10 times the content of other muscle tissues. Wheat, peanuts, bean sprouts, fresh vegetables, and fruits all contain rich vitamin B. The intake of vitamin A mainly comes from carrots, green leaves, and milk. , Cod liver oil, animal liver, etc .; and vitamin C mainly comes from fresh fruits and vegetables, especially hawthorn, mandarin, orange. Therefore, the above fruits, vegetables, and meat can be eaten more to supplement enough vitamins.

4. Low fat: Fat can provide body heat and certain fatty acids and fat-soluble vitamins, and can promote appetite. Generally, patients can eat 40-60 grams of fat daily. Fat metabolism requires bile from the liver, and bile can break down fat into fine particles that can be absorbed. However, when suffering from acute hepatitis, the bile secretion is insufficient due to liver inflammation, which reduces the digestion and absorption capacity of fat. Eating a lot of high-fat substances and forcing the liver to secrete bile will increase the burden on the liver and make the disease worse. Therefore, in the acute hepatitis period, you should eat less fat-containing substances to the extent that patients can tolerate without affecting appetite and digestion. When jaundice subsides and appetite increases, edible and digestible fats with low cholesterol, such as vegetable oils and creams, can be consumed if too much intake will affect digestion and absorption of the spleen and stomach, as well as bloating, diarrhea, and liver cells. Internal fat deposition can prevent the synthesis of liver glycogen, which can lead to fatty liver and reduce the physiological function of liver cells.

In addition, patients with acute hepatitis also need to pay attention to fasting spicy food, cold food, smoking and alcohol, so as not to increase the burden on the liver, which is not conducive to the recovery of the disease.

Acute hepatitis expert opinion

When suffering from acute hepatitis, or some symptoms of the above-mentioned acute hepatitis, don't take it lightly and don't fuss about it. As long as you go to a regular medical institution for treatment, the timely treatment is appropriate, and acute hepatitis can be completely cured. Don't get sick and consult a doctor.