Elderly viral hepatitis

　　The main cause of viral hepatitis is hepatitis virus infection. The etiological classification of viral hepatitis, currently recognized, includes five types of hepatitis viruses: hepatitis A (HAV), hepatitis B (HBV), hepatitis C (HCV), hepatitis D (HDV), and hepatitis E (HEV). Among them, hepatitis B virus is a DNA virus, while the others are RNA viruses. Hepatitis G has been reported, but the pathogen has not been successfully isolated to date. The relationship between the hepatitis G virus, which belongs to the Flaviviridae and is a single-stranded DNA, and human hepatitis, as determined by representative difference analysis in recent years, is still controversial.

　　Elderly hepatitis is mainly caused by hepatitis B, followed by hepatitis C, with a high rate of co-infection of 2 or more hepatitis viruses, and hepatitis A is rare.

　　The pathophysiological changes caused by various hepatitis viruses in hepatitis, except for hepatitis A and E, are basically the same. The basic pathological characteristics are: liver cell degeneration, necrosis, apoptosis, regeneration, infiltration of inflammatory cells, and proliferation of stroma (extracellular matrix). Acute hepatitis is mainly characterized by inflammation, degeneration, and necrosis, with不明显fibrosis. Chronic hepatitis shows varying degrees of liver cell necrosis and inflammation, mainly in the portal area, around the portal area, and in the liver lobules. Severe lesions may have destruction of liver lobular structure, fibrosis, and nodular regeneration, forming liver cirrhosis. Acute jaundice type hepatitis is characterized by a large number of liver cell necrosis without fibrous tissue proliferation. Subacute severe hepatitis, in addition to a large number of liver cell necrosis, shows liver cell regeneration and collagen fibers, forming regeneration nodules. Chronic severe hepatitis appears on the basis of chronic hepatitis and liver cirrhosis, with pathophysiological changes of subacute severe hepatitis. The pathological changes of cholestatic hepatitis are marked intravascular congestion of bile, and the formation of bile thrombi on the basis of acute hepatitis lesions.

　　Elderly viral hepatitis not only causes general discomfort, decreased appetite, and abdominal distension in patients, but severe cases may have deepening jaundice, ascites, lower limb edema, bleeding tendency, and can complicate with portal hypertension, bleeding tendency, hepatic encephalopathy, liver cirrhosis, and other complications.

　　According to the program for the prevention and treatment of viral hepatitis, elderly viral hepatitis can be divided into 5 clinical types.

　　1. Acute hepatitis
　　It is divided into acute jaundice type hepatitis and acute non-jaundice type hepatitis, with an incubation period of 15 to 45 days, with an average of 25 days, and a total course of 2 to 4 months.
　　1. Pre-jaundice period: Symptoms include chills, fever, fatigue, decreased appetite, nausea, aversion to fatty food, abdominal discomfort, and pain in the liver area, urine color gradually deepens, this period lasts an average of 5 to 7 days.
　　2. Jaundice period: Fever subsides, the conjunctiva and skin turn yellow, jaundice appears, and自觉 symptoms improve, liver enlargement, accompanied by tenderness and percussion pain, partial mild splenomegaly, this period lasts 2 to 6 weeks.
　　3. Recovery period: Jaundice gradually subsides, symptoms decrease and disappear, the liver and spleen shrink, liver function gradually returns to normal, this period lasts from 2 weeks to 4 months, with an average of 1 month.

　　2. Chronic hepatitis
　　Previous history of hepatitis B, C, D, or HBsAg carrier status, or acute hepatitis course lasting more than half a year, with ongoing hepatitis symptoms, signs, and abnormal liver function can be diagnosed as chronic hepatitis. Common symptoms include fatigue, general discomfort, decreased appetite, discomfort or pain in the liver area, abdominal distension, and low fever. Signs include dark complexion, jaundice of the conjunctiva, possible spider veins or liver palms, liver enlargement, moderate or full texture, and tenderness and percussion pain, with frequent splenomegaly. Severe cases may have deepening jaundice, ascites, lower limb edema, bleeding tendency, and hepatic encephalopathy. To reflect the degree of liver damage, clinical classification can be made:
　　1. Mild: The condition is mild, symptoms are not obvious, or there are symptoms and signs, but biochemical indicators only show 1-2 mild abnormalities.
　　2. Moderate: Symptoms, signs, and laboratory findings are between mild and severe.
　　3. Severe: There are obvious or persistent hepatitis symptoms, such as fatigue, anorexia, abdominal distension, and loose stools. It may be accompanied by signs of liver disease, such as facial ecchymosis, palmar erythema, spider angioma, or splenomegaly, excluding other causes and without portal hypertension. Laboratory examination shows recurrent or persistent elevation of serum alanine aminotransferase: reduced albumin or abnormal A/G ratio, significantly increased gamma globulin. If any one of the following three tests (albumin ≤ 32g/L, bilirubin > 85.5μmol/L, prothrombin activity 60% ~ 40%) is detected, it can be diagnosed as severe chronic hepatitis.

　　III. Severe hepatitis
　　1. Acute severe hepatitis: Onset is acute, with rapid progression, deep jaundice, small liver, and rapid onset of neurological and psychiatric symptoms (hepatic encephalopathy grade II or above) within 10 days after onset. Bleeding tendency is obvious, and symptoms such as liver odor, ascites, and hepatorenal syndrome may occur. If the prothrombin activity is below 40% and other causes are excluded, cholesterol is low, and liver function is significantly abnormal.
　　2. Subacute severe hepatitis: After 10 days of onset, there is still extreme fatigue, anorexia, severe jaundice (bilirubin > 171 μmol/L), abdominal distension, and the formation of ascites, with frequent obvious bleeding phenomena. Generally, liver shrinkage is not prominent, and hepatic encephalopathy is more common in the later stage. Severe liver function damage: serum ALT is elevated, or it is not significantly elevated but total bilirubin is significantly elevated, i.e., bilirubin-separation, A/G ratio inversion, increased gamma globulin, prolonged prothrombin time, and prothrombin activity < 40%.
　　3. Chronic severe hepatitis: Patients with chronic hepatitis, liver cirrhosis, or a history of carrying the hepatitis B surface antigen, or those without the above history but with chronic hepatitis manifestations supported by imaging, laparoscopic examination, or liver biopsy, and presenting with clinical manifestations and laboratory changes of subacute severe hepatitis are diagnosed as chronic severe hepatitis.

　　IV. Cholestatic hepatitis
　　The onset is similar to acute jaundice hepatitis, but the自觉 symptoms are usually mild, with obvious liver enlargement, skin itching, pale stools, and significant increases in serum alkaline phosphatase, γ-glutamyl transpeptidase, and cholesterol. Jaundice is deep, and the increase in bilirubin is mainly direct. Gastrointestinal symptoms are not obvious, the rise in transaminases is small, and the prothrombin time and prothrombin activity are normal. The characteristic is the discrepancy between mild clinical symptoms and deep jaundice.

　　V. Post-hepatitis liver cirrhosis
　　Early liver cirrhosis is difficult to diagnose solely based on clinical data and must rely on pathological diagnosis, imaging diagnosis (ultrasound, CT, etc.), and laparoscopic examination for the most reference value. Clinical diagnosis of liver cirrhosis refers to chronic hepatitis patients with evidence of portal hypertension, such as varicose veins in the abdominal wall and esophagus, ascites, imaging findings of liver shrinkage, splenomegaly, and widened diameters of the portal vein and splenic vein, and excluding other causes that can cause portal hypertension. Liver cirrhosis is divided into active and inactive types according to the degree of hepatitis activity. For elderly hepatitis patients, attention should be paid to the following aspects on the basis of the above five clinical types:
　　1. The onset is often atypical: Due to the decline in physiological and immune functions in the elderly, some elderly viral hepatitis patients may have been infected with chronic hepatitis or become chronic carriers. Once the resistance decreases, symptoms become more severe and the disease develops. Severe hepatitis and complications occur more frequently in elderly hepatitis, and the mortality rate is also high. People with a drinking habit are more prone to hepatitis B and C, and these two types of hepatitis often lead to chronic hepatitis and liver cirrhosis. Some may develop into hepatocellular carcinoma.
　　2. The clinical symptoms of elderly hepatitis are more severe: In addition to fatigue, nausea, and abdominal distension, there is liver enlargement, more frequent occurrence of jaundice, deeper jaundice, and slower regression. Cholestatic hepatitis is also more common.
　　3. Elderly viral hepatitis often has a very deep jaundice: Sometimes, due to atypical symptoms, it is difficult to distinguish from extrahepatic obstructive jaundice, such as gallstones or liver cancer, pancreatic head cancer, and bile duct cancer. Therefore, in addition to biochemical tests related to liver function and the hepatitis antigen-antibody system, B-ultrasound or CT examination may be used sometimes.
　　4. More complications: Elderly people often have various chronic diseases, such as hypertension, coronary heart disease, chronic tracheitis, emphysema, etc. The resistance of the elderly is also low, which may affect diagnosis. For example, when heart failure is accompanied by hepatitis, it should be distinguished from liver function abnormalities caused by heart failure itself.

　　Viral hepatitis is a communicable disease. Elderly people have poor resistance, so they should be particularly cautious about preventing infection in daily life.

　　1. Manage the source of infection

　　Isolate acute hepatitis A patients until the infectivity is gone. People with chronic hepatitis and asymptomatic HBV, HCV carriers should be prohibited from donating blood and engaging in food service, child care, and other work. For patients with HBV marker-positive liver disease, treatment and management guidance should be given according to their symptoms, signs, and laboratory examination results.

　　2. Cut off the route of transmission

　　Focus on preventing fecal-oral transmission of hepatitis A and E, strengthening water source protection, food and personal hygiene, and strengthening fecal management. Focus on preventing the transmission through blood and body fluids for hepatitis B, C, and D. Strengthen the screening of blood donors, strictly control the application of blood transfusion and blood products. If there is a possibility of wound or needlestick infection with hepatitis B virus, high-titer hepatitis B immune globulin can be used. Syringes and invasive examination and treatment instruments should be strictly disinfected to control mother-to-child transmission.

　　3. Protect susceptible populations

　　Artificial immunity, especially active immunity, is the fundamental measure for preventing hepatitis. However, due to genetic heterogeneity, there is still no vaccine that can be widely applied for some hepatitis viruses (such as HCV). The hepatitis A vaccine has been put into use, and the hepatitis B vaccine has been promoted in China, achieving good results. For infants born to HBsAg and HBeAg-positive pregnant women, high-titer hepatitis B immune globulin (HBIG) should be injected within 24 hours of birth, and a hepatitis B vaccine should be administered at the same time. One month after birth, HBIG and the vaccine should be injected again.

　　The clinical examination of elderly viral hepatitis is mainly divided into three aspects.

　　Firstly, liver function detection

　　1. Serum Enzyme Detection

　　Alanine aminotransferase (ALT) is 10,000 times higher in liver cells than in serum. If 1% of liver cells die, the serum concentration can increase by a factor of 1. The positive rate of acute hepatitis is 80% to 100%, but it lacks specificity. Aspartate aminotransferase (AST) has the highest concentration in the myocardium, so when evaluating the impact on liver function, it is first necessary to exclude the impact of heart disease. AST is present in 80% of liver cell mitochondria. Generally, liver injury is mainly characterized by an increase in ALT. If the serum AST is significantly increased, it often indicates severe necrosis of liver cells, with AST released into the blood from the mitochondria. The degree of increase in serum transaminases is roughly proportional to the severity of the lesion, but in severe hepatitis, it can appear that bilirubin continues to increase while transaminases decrease, which is called 'bile enzyme dissociation' and is the result of almost complete necrosis of liver cells.

　　2. Serum Protein Detection

　　In clinical practice, serum protein is often used as a biochemical indicator of liver protein metabolism. In chronic hepatitis and liver cirrhosis, there is often a decrease in serum albumin and an increase in globulin levels, with γ-globulin increasing predominantly.

　　3. Serum Bilirubin Detection

　　The liver has the functions of uptake, transport, binding, and excretion in the metabolism of bilirubin. Liver function injury leads to an increase in bilirubin levels. In addition to cholestatic hepatitis, the level of bilirubin is proportional to the severity of liver injury.

　　4. Prothrombin Time (PT)

　　It can sensitively reflect the situation of liver synthesis of coagulation factors II, VII, IX, and X. The length of PT in liver disease is positively correlated with the degree of liver injury.

　　Secondly, detection of hepatitis virus markers

　　1. Hepatitis A

　　Acute hepatitis patients with a positive anti-HAVIgM in serum can be diagnosed with recent HAV infection. A positive anti-HAV-IgG indicates previous infection and the presence of immunity.

　　2. Hepatitis B

　　(1) HBsAg and anti-HBs: A positive HBsAg indicates that HBV is currently in the infection stage. Anti-HBs is an immunoprotective antibody, and a positive result indicates that immunity against HBV has been produced. The diagnosis of chronic HBsAg carriers is based on the absence of any clinical symptoms and signs, normal liver function, and a sustained positive HBsAg for more than 6 months.

　　(2) HBeAg and anti-HBe: A positive HBeAg is an indicator of active replication and strong infectivity of HBV. The conversion of the tested serum from HBeAg-positive to anti-HBe-positive indicates that the disease has缓解ed and the infectivity has decreased.

　　(3) HBcAg and anti-HBc: A positive HBcAg indicates the presence of intact HBV particles, directly indicating active replication of HBV. Due to the complexity of the detection method, it is rarely used in clinical practice. Anti-HBc is a marker for HBV infection, and a positive anti-HBcIgM indicates an early stage of infection, with viral replication in the body. In patients with chronic mild hepatitis B and HBsAg carriers, all three HBsAg, HBeAg, and anti-HBc are positive, indicating a high degree of infectivity, and it is difficult for the indicators to become negative.

　　Molecular biology marker: Detection of HBV DNA in serum by molecular hybridization or PCR, a positive result directly indicates active replication of HBV and its infectiousness.

　　3. Hepatitis C

　　Hepatitis C cannot be detected due to the very low amount of antigen in the blood, so antibodies can only be detected. Anti-HCV is a marker for HCV infection and is not a protective antibody. Detection of HCV-RNA in serum using nested reverse transcription PCR indicates active viral replication and infectivity.

　　4. Hepatitis D

　　HDV is a defective virus that depends on HBsAg for replication and can manifest as simultaneous infection with HDV and HBV. HDAg appears in the blood for only a few days, followed by the appearance of IgM-type anti-HD. Chronic HDV infection is characterized by a sustained increase in anti-HDIgG levels. The detection of HDV-RNA in serum is a more direct and specific diagnostic method.

　　5. Hepatitis E

　　Antibodies against HEV IgM are detected in the serum of acute hepatitis patients, and the titer of IgG antibodies in convalescent serum is very low. The duration of anti-HEV IgG in serum is less than 1 year, so both anti-HEV IgM and anti-HEV IgG can serve as indicators of recent HEV infection.

　　6. Hepatitis G

　　RT-PCR technology can detect HGV RNA, which is an effective method for the early diagnosis and monitoring of viremia in HGV. The IgM and IgG antibodies against HGV are not yet mature, characterized by low detection rates and inconsistency with the results of RT-PCR.

　　Three, Liver biopsy with living tissue examination

　　It is a major indicator for diagnosing various types of viral hepatitis and also serves as a definite evidence for early diagnosis of liver cirrhosis. However, due to its traumatic nature, it has not been widely adopted and is not considered the first choice.

　　The diet for elderly patients with viral hepatitis should be as follows:

　　1. Ensure an adequate supply of calories, with an intake of 8400-10500 kilojoules (2000-2500 calories) per day being more appropriate. The high-calorie therapy for hepatitis that was previously advocated is not advisable, as high calories can improve clinical symptoms but can ultimately lead to fatty liver, which can worsen the condition, so the disadvantages outweigh the benefits.

　　2. Carbohydrates can generally account for 60-70% of total energy intake. The high-sugar diet that was previously adopted should be corrected, as high-sugar diets, especially excessive glucose, fructose, and sucrose, can affect the appetite of patients, worsen gastrointestinal bloating, increase fat storage in the body, and lead to obesity and fatty liver. The supply of carbohydrates should mainly come from staple foods.

　　3. To promote the repair and regeneration of liver cells, an increased supply of protein should be provided, which should generally account for 15% of total energy intake. It is especially important to ensure a certain amount of high-quality protein, such as animal protein and soy products.

　　4. There is generally no need to limit fat intake, as hepatitis patients often have symptoms such as aversion to oil and loss of appetite. Under normal circumstances, there will not be an excessive intake of fat.

　　5. Ensure the supply of vitamins. B vitamins such as vitamin B1, vitamin B2, niacin, and vitamin C play an important role in improving symptoms. In addition to choosing foods rich in these vitamins, oral administration of various vitamin preparations can also be considered.

　　6. Ensure an adequate supply of liquid. Drinking more fruit juice, rice gruel, honey water, watermelon juice, and other beverages can accelerate the excretion of toxins and ensure the normal metabolic function of the liver.

　　7, Pay attention to cooking methods, enhance the color, smell, taste, and shape of food to promote appetite. Avoid fried and baked foods and strongly刺激性 foods, limit high-nitrogen extract foods such as meat soup and chicken soup, to reduce the burden on the liver.

　　8, Eat in small and frequent meals.

　　The physical quality of elderly people is poor, their resistance is weak, and they often have chronic metabolic diseases such as hypertension, coronary heart disease, and diabetes. Therefore, timely treatment is required after elderly people are infected with hepatitis virus to avoid the difficulty of treatment when the condition develops into liver cirrhosis and other diseases.

　　First, routine treatment

　　1, General treatment: Acute hepatitis and active stage chronic hepatitis require hospitalization for treatment, bed rest, reasonable nutrition, ensuring the supply of calories, proteins, and vitamins, and strictly prohibiting alcohol consumption. During the recovery period, activities should be gradually increased. For chronic hepatitis in a stationary phase, work that can be done is possible. For severe hepatitis, absolute bed rest is required, and protein intake in the diet should be minimized, ensuring calories and vitamins, and albumin or fresh plasma can be administered to maintain water and electrolyte balance.

　　2, Antiviral therapy: Antiviral treatment is generally not used for acute hepatitis, but early interferon application is recommended for acute hepatitis C to prevent chronicity. For chronic viral hepatitis, antiviral treatment is needed.

　　①Interferon: Recombinant DNA leukocyte interferon (IFN-α) can inhibit the replication of HBV. Intramuscular injection of 3 million to 5 million U every other day for continuous 6 months, only 30% to 50% of patients achieve a relatively sustained effect. The activity of DNA polymerase, HBeAg, and HBV-DNA can sequentially become negative, transaminase tends to normal, and changes in liver tissue can be improved. However, it is difficult to maintain the negative conversion of HBsAg. Some patients may see the activity of DNA polymerase rise again after discontinuation of medication, and the efficacy cannot be consolidated. Interferon is the first-line drug for chronic hepatitis C, and can be used in combination with ribavirin. The side effects of interferon can include fever, chills, malaise, nausea, vomiting, diarrhea, hypotension, myalgia, headache, hair loss, and bone marrow suppression, but the incidence rate is low.

　　②Lamivudine: It is a synthetic deoxyuridine nucleoside drug with the effect of anti-HBV. Its mechanism is to inhibit HBV DNA polymerase and can competitively incorporate into the HBV DNA chain with cytidine (LTP), terminate DNA chain synthesis, and inhibit the replication of HBV-DNA. Oral administration of 100mg/day of lamivudine for 2-4 weeks can significantly reduce the level of HBV-DNA in serum. After 12 weeks of medication, the rate of HBV-DNA negativity reaches over 90%. Long-term use can reduce ALT and improve liver inflammation. However, the negative conversion rate of HBeAg is only 16%-18%. Variations of HBV can occur after treatment for more than 6 months, but the medication can still be continued. The side effects of this drug are mild and can be continued for 1-4 years.

　　③Famciclovir: It is a guanine analog drug with a long half-life and high concentration in cells, which can inhibit the replication of HBV-DNA. Method: 500mg, 3 times a day, for a total of 16 weeks. The side effects of this drug are mild and can be used in combination with lamivudine, interferon, and other drugs to improve efficacy.

　　④ Other antiviral drugs, such as acyclovir, adefovir, foscarnet sodium, etc., all have a certain inhibitory effect on HBV.

　　3. Immune modulators:

　　① Thymosin α1 (Rituximab): It has a bidirectional immune regulatory effect. It can rebuild the immune function of primary and secondary immune deficiency patients. Dosage: 1.6mg/time, 2 times a day, subcutaneous injection, the course of treatment is 6 months.

　　② Thymosin: It participates in the immune response of the body's cells, induces the differentiation and maturation of T lymphocytes, amplifies the response of T cells to antigens, and regulates the balance of various subpopulations of T cells. Dosage: 20-30mg/d, intravenous infusion, 2-3 months as a course.

　　③ Immune ribonucleic acid: It can induce interferon in the body and enhance the immune function of the body. 100-300mg added to 250mg of 5% glucose or normal saline for intravenous infusion.

　　4. Guided treatment: New immunotherapy (such as DNA vaccine, immunocomplex therapy, etc.), gene therapy (antisense nucleic acid therapy, gene transfer therapy) are under study.

　　5. Liver-protecting drugs:

　　① Hepatocyte growth factor: It can stimulate the synthesis of normal liver cell DNA, promote liver cell regeneration, protect liver cells from damage, promote the repair of pathological cells, and regulate the immune function and antifibrotic effect of the body. Chronic hepatitis: 40-80mg added to 10% glucose solution for intravenous infusion, once a day, the course of treatment is 1-3 months.

　　② Silymarin: It has the effect of protecting and stabilizing the liver cell membrane and can be taken orally for 1-3 months.

　　③ Glycyrrhizin disodium (Ganlixin): It has strong anti-inflammatory, protective cell membrane, and liver function improvement effects. It is suitable for chronic hepatitis with elevated alanine aminotransferase. Dosage: Oral 150mg/time, 3 times a day; intravenous infusion 30-50ml added to 250ml of 10% glucose or normal saline, once a day, the course of treatment is 2-8 weeks.

　　④ Adenosine methionine (Simmetil): It is a compound produced by methionine and adenosine triphosphate (ATP) under the action of adenosine methionine enzyme. Viral hepatitis can cause endogenous deficiency of adenosine methionine, affecting cell metabolism, leading to intrahepatic bile stasis, damaging liver cells, and supplementing exogenous adenosine methionine has the effect of promoting jaundice regression and liver function recovery.

　　6. Traditional Chinese medicine:辨证treatment has a good effect on improving symptoms and liver function, such as Artemisia, Gardenia,芍药,丹参, etc.

　　Second, optimal treatment plan

　　1. For acute severe and chronic severe hepatitis: ① Patients should rest in bed, ensure calorie, protein, and vitamin supply. ② Glucose and vitamin C can be administered intravenously. ③ Hepatocyte growth factor: 80-120mg added to 10% glucose solution for intravenous infusion, once a day, the course of treatment is generally 1 month. ④ For those with severe jaundice, adenine methionine (Simmetil) can be added, 1000mg added to 250ml of 10% glucose solution for intravenous infusion, once a day, the course of treatment is 20 days to 1 month. ⑤ For those with hepatic encephalopathy, arginine and hexapeptide are administered intravenously.

　　2. Chronic hepatitis: Compound Danshen and Astragalus are infused to promote blood circulation and remove blood stasis, improve immune function, and promote the regeneration of liver cells. Dosage: 20 mg of Compound Danshen and 40 g of Astragalus are added to 250 ml of 10% glucose for intravenous infusion, with a course of treatment of 30 days.

　　Three, Antiviral Treatment

　　Currently, it is believed that the efficacy of interferon alpha alone is not satisfactory for chronic hepatitis, and it is advocated to be used in combination with immunomodulators, and it can also be used in combination with other antiviral drugs.

　　1. Treatment of Hepatitis B:

　　① Interferon plus Thymosin (Rebetol): Interferon 5 million U, injected intramuscularly every other day, Thymosin (Rebetol) 1.6 mg per dose, injected subcutaneously twice a week, course of treatment 4 to 6 months.

　　② Interferon plus Lamivudine: Lamivudine can be taken orally at 100 mg per day for 1 to 4 years.

　　③ Lamivudine plus Sophora Flavescens Alkaloid (Bortetili): Sophora Flavescens Alkaloid is a bioalkaloid extracted from the natural plant Sophora flavescens, which has the effects of directly antagonizing hepatitis B virus, regulating immunity, protecting liver cells, and preventing and treating liver fibrosis. 600 mg, once a day, injected intramuscularly for 45 days, 400 mg, once a day, injected intramuscularly for 45 days, course of treatment 3 months.

　　2. Treatment of Hepatitis C:

　　① Interferon plus Ribavirin (Virazole): Interferon 3 to 5 million U, injected intramuscularly every other day, course of treatment 12 to 18 months.

　　② Interferon plus Thymosin (Rebetol): Interferon 3 million U, injected intramuscularly every other day, Thymosin (Rebetol) 1.6 mg per dose, injected subcutaneously twice a week.

　　Four, Rehabilitation Treatment

　　Even after the improvement of viral hepatitis, a light diet is still needed, and vitamins should be rich in order to ensure calories and avoid excessive food intake to increase the burden on the liver.

　　Hepatitis A, with a generally good prognosis. Chronic hepatitis B and hepatitis B have poor prognoses, most of which are persistent and a few develop into liver cirrhosis. Hepatitis C is more likely to develop liver cirrhosis and liver cancer. HEV infection does not become chronic, but the overall mortality rate is higher than that of hepatitis A.