Viral hepatitis B, or hepatitis B for short, is a disease caused by the hepatitis B virus (HBV) that infects the body. Hepatitis B virus is a hepatophilic virus that mainly exists in liver cells and damages them, causing inflammation, necrosis and fibrosis. There are two types of viral hepatitis B: acute and chronic. Acute hepatitis B is self-resolving in 90% of adults. The transmission of hepatitis B: hepatitis B is a blood-borne disease, mainly through blood (such as unsafe injection history, etc.), mother-to-child transmission and sexual transmission, skin and mucous membrane breakage transmission also has a certain proportion, such as tattoos, ear piercing, endoscopy, etc. Blood products are now strictly controlled, the possibility of transmission is greatly reduced, irregular transfusion of blood and blood products only when it occurs. Accidental exposure in the work of medical personnel should not be ignored. With the vigorous promotion of hepatitis B vaccine in newborns and the implementation of other mother-to-child interruption measures, mother-to-child transmission has been greatly controlled. HBV infection is not transmitted through the respiratory and digestive tracts, so daily study, work or living contacts, such as sharing the same office (sharing office supplies such as computers), living in the same dormitory, eating in the same restaurant, hugging, shaking hands, sharing toilets, etc., will not be infected with HBV. Epidemiological and experimental studies have not found that hepatitis B can be transmitted by blood-sucking insects, such as mosquitoes and bedbugs bites. The classification of hepatitis B: 1, according to the length of disease classification: hepatitis B can be divided into acute hepatitis B and chronic hepatitis B, determine whether it is acute or chronic hepatitis B in the clinical diagnosis and treatment is very important, the two treatment principles are different, the prognosis is also very different, sometimes in order to distinguish between acute and chronic hepatitis, often through liver penetration pathological examination to determine. Acute hepatitis B is a self-limiting disease that often does not require antiviral therapy. Patients with HBsAg(+) in the blood for less than 6 months, hepatitis B virus cleared by the body’s immune system within 6 months, HBsAg negative, may be left with serological signs of having been infected with HBV: three antibodies positive for HBe, anti-HBe and anti-HBS, but the appearance of anti-HBS is late in some patients. Low levels may also not be high. The key feature of acute hepatitis B is negative HBsAg within six months. In contrast, chronic hepatitis B is, in a word, the presence of HBV in the body for more than 6 months. 2, according to the severity of the classification: can be divided into hepatitis B carriers, active hepatitis B, heavy hepatitis, hepatitis cirrhosis, which hepatitis B carriers are divided into chronic HBV-DNA carriers (major triplets, high levels of quantitative DNA but normal liver function in the immune tolerance state patients), inactive HBsAg carriers (minor triplets, HBV-DNA below the lower limit of detection, normal liver function); active Hepatitis B is also divided into e antigen-positive chronic hepatitis B and e antigen-positive chronic hepatitis B; hepatitis cirrhosis is also divided into compensated cirrhosis and decompensated cirrhosis; heavy hepatitis can be divided into acute heavy, subacute heavy and chronic heavy hepatitis. 3, according to the presence or absence of jaundice (that is, according to the characteristics of the symptoms), can be divided into jaundice type and non-jaundice type, the classification is mostly for acute hepatitis B, that is, acute jaundice hepatitis B and acute non-jaundice hepatitis B. What kind of hepatitis B needs treatment? 1. HBV-DNA greater than 103copies/L; 2. Abnormal liver function; 3. Positive surface antigen. Treatment: 1, the overall goal of treatment The overall goal of treatment of chronic hepatitis B is to maximize long-term HBV, reduce hepatocellular inflammatory necrosis and liver fibrosis, delay and reduce the occurrence of liver decompensation, cirrhosis, HCC and its complications, thereby improving quality of life and prolonging survival time. 2, general indications for antiviral therapy General indications include: (1) HBeAg positive, HBV-DNAR 105 copies/ml (equivalent to 20,000 IU/ml); HBeAg negative, HBV-DNAR 104 copies/ml (equivalent to 2,000 IU/ml); (2) ALTR2×ULN. If treated with IFN, ALT should Q10×ULN and total serum bilirubin should be 2×ULN; (3) ALT2×ULN, but liver histology shows KnodellHAIR4, or inflammatory necrosis RG2, or fibrosis RS2. Antiviral therapy should also be considered for those who are persistently HBV-DNA positive and do not meet the above treatment criteria, but have one of the following conditions: (1) For those with ALT greater than ULN and age (2) For those with persistently normal ALT but older (40 years old), close follow-up, preferably with liver tissue biopsy, should be considered; if liver histology shows KnodellHAIR4, or inflammatory necrosis RG2, or fibrosis RS2, antiviral therapy should be actively administered; (3) For those with evidence of disease progression (e.g., enlarged spleen) on dynamic observation liver histology is recommended, and antiviral therapy should be given if necessary (. Before starting treatment, ALT elevation due to drugs, alcohol or other factors should be excluded, as well as temporary normalization of ALT after application of enzyme-lowering drugs. In some special diseases such as cirrhosis or taking biphenyl structured derivatives, the AST level may be higher than the ALT, and the AST level may be used as the main indicator at this time. IFNα treatment China has approved both regular IFNα (2a, 2b and 1b) and pegylated interferon α (2a and 2b) [PegIFNα (2a and 2b)] for the treatment of chronic hepatitis B. The results of the meta-analysis showed that patients with chronic hepatitis B treated with regular IFN had better HBeAg serological conversion rates, HBsAg disappearance rates, cirrhosis incidence rates, and HCC incidence rates than those without IFN treatment. The results of clinical trials on HBeAg-negative patients suggest that a course of common IFNα for at least 1 year is required to achieve better outcomes. The results of international multicenter randomized controlled clinical trials showed that HBeAg-positive chronic hepatitis B patients (87% Asian) treated with PegIFNα-2a for 48 weeks had a HBeAg seroconversion rate of 32% at 24 weeks of discontinuation follow-up; the HBeAg seroconversion rate was up to 43% at 48 weeks of discontinuation follow-up. The results of foreign studies showed that similar rates of HBV-DNA resistance, HBeAg serological conversion and HBsAg disappearance were achieved with PegIFNα-2b in HBeAg-positive chronic hepatitis B patients. In HBeAg-negative chronic hepatitis B patients (60% Asian) treated with PegIFNα-2a for 48 weeks, the rate of HBV-DNA 104 copies/ml (equivalent to 2000 IU/ml) was 43% at 24 weeks post-discontinuation and 42% at 48 weeks post-discontinuation; the rate of HBsAg disappearance was 3% at 24 weeks post-discontinuation and increased to 8% at 3 years post-discontinuation. The rate of HBsAg disappearance was 3% at 24 weeks of discontinuation and increased to 8% at 3 years of discontinuation. 1, IFN antiviral efficacy predictors with the following factors can often achieve better results: (1) high levels of ALT before treatment; (2) HBV-DNA 2 × 108 copies/ml (equivalent to 4 × 107IU/ml); (3) female; (4) short duration of disease; (5) non-maternal-to-child transmission; (6) heavy inflammatory necrosis of liver tissue, fibrosis is light; (7) good compliance with treatment (8) no co-infection with HCV, HDV or HIV; (9) HBV genotype A; (10) undetectable serum HBV-DNA at 12 or 24 weeks of treatment (II). Among them, pre-treatment ALT, HBV-DNA levels and HBV genotype, are important factors to predict the efficacy. In the results of the study, the quantitative detection of HBsAg level or HBeAg level has a good predictive value for treatment response during PegIFNα-2a treatment. 2. Monitoring and follow-up of IFN treatment Before treatment, the following should be checked: (1) biochemical indicators, including ALT, AST, bilirubin, albumin and renal function; (2) routine blood, urine, glucose and thyroid function; (3) virological markers, including baseline status or levels of HBsAg, HBeAg, anti-HBe and HBV-DNA; (4) for patients above middle age, the (5) Exclude autoimmune diseases; (6) Urine human chorionic gonadotropin test to exclude pregnancy. (2) Biochemical indexes: including ALT and AST, should be tested once a month for 3 consecutive times after the start of treatment, and once every 3 months afterwards as the disease improves; (3) Viral markers: HBsAg and AST should be tested once every 3 months after the start of treatment. (3) Viral markers: HBsAg, HBeAg, anti-HBe and HBV-DNA should be tested once every 3 months after the start of treatment; (4) Other: thyroid function, blood glucose and urinary routine should be tested once every 3 months; if thyroid function is abnormal or diabetes is already present before treatment, thyroid function abnormalities or diabetes should be controlled with drugs before starting IFN treatment, and thyroid function and blood glucose levels should be checked monthly; (5) Regular assessment should be made. (5) Mental status should be evaluated regularly: patients with significant depression and suicidal tendencies should be immediately discontinued and closely monitored. 3, IFN adverse reactions and their management (1) flu-like syndrome: manifested as fever, chills, headache, muscle aches and weakness, etc., can be injected at bedtime IFNα, or take antipyretic and analgesic drugs at the same time as IFN. (2) Transient peripheral cytopenia: mainly manifests as a decrease in peripheral blood leukocytes (neutrophils) and platelets. If the absolute neutrophil count Q0.75×109/L and/or platelets 50×109/L, the dose of IFNα should be reduced; recheck after 1 to 2 weeks, and if recovery, gradually increase to the original amount. If the absolute neutrophil count Q0.5×109/L and/or platelets 30×109/L, the drug should be discontinued. For those with significantly lower neutrophils, granulocyte colony-stimulating factor (G-CSF) or granulocyte macrophage colony-stimulating factor (GM-CSF) therapy can be tried (III). (3) Psychiatric abnormalities: may manifest as depression, delusions, severe anxiety and other symptoms of mental illness. For those with severe symptoms, IFNα should be discontinued promptly, and further consultation with a neuropsychiatrist if necessary. (4) Autoimmune diseases: some patients may develop autoantibodies, only a small number of patients develop thyroid disease (hypothyroidism or hyperthyroidism), diabetes, thrombocytopenia, psoriasis, leukoplakia, rheumatoid arthritis and systemic lupus erythematosus-like syndrome, etc., which should be treated by consultation with physicians of relevant departments, and the drug should be discontinued in serious cases. (5) Other rare adverse reactions: including renal damage (interstitial nephritis, nephrotic syndrome and acute renal failure, etc.), cardiovascular complications (arrhythmia, ischemic heart disease and cardiomyopathy, etc.), retinopathy, hearing loss and interstitial pneumonia, etc., IFN therapy should be discontinued. 4. Contraindications to IFN therapy Absolute contraindications to IFN therapy include: pregnancy, history of psychiatric disorders (such as major depression), uncontrolled epilepsy, unabstained alcohol or drug abusers, uncontrolled autoimmune diseases, decompensated cirrhosis, and symptomatic heart disease. Relative contraindications to IFN therapy include thyroid disease, retinopathy, psoriasis, previous history of depression, uncontrolled diabetes, hypertension, pre-treatment neutrophil count of 1.0 x 109/L and/or platelet count of 50 x 109/L , and total bilirubin of 51 μmol/L (especially in those with predominantly indirect bilirubin). Nucleoside (acid) drug therapy 1, nucleoside (acid) drugs Currently there are five anti-HBV nucleoside (acid) drugs that have been used in clinical practice, four of which have been marketed in China. (1) lamivudine: 100mg of lamivudine taken orally once a day can significantly inhibit HBV DNA levels. Patients with chronic hepatitis B with marked liver fibrosis and compensated cirrhosis treated with lamivudine for 3 years can delay disease progression and reduce the incidence of hepatic decompensation and HCC. Patients with decompensated cirrhosis also improved liver function and prolonged survival after treatment with lamivudine. Lamivudine has a low incidence of adverse reactions and a safety profile similar to that of placebo. The incidence of viral resistance mutations increased with longer treatment duration (14%, 38%, 49%, 66% at years 1, 2, 3, and 4, respectively). (2) Adefovir: Oral adefovir in patients with chronic hepatitis B significantly inhibited HBV DNA replication, promoted ALT normalization, and improved inflammatory necrosis and fibrosis of liver tissue. The cumulative incidence of drug resistance mutations in patients at 5 years of treatment was 29%, the incidence of virologic resistance was 20%, and the incidence of clinical resistance was 11%; the incidence of mild creatinine elevation was 3%. The incidence of resistance to adefovir is lower with adefovir combined with lamivudine. (3) Entecavir: a nucleoside analog with potent and rapid inhibition of viral replication, one 0.5 mg tablet daily for initial treatment. long-term follow-up studies have shown that for those who achieve virological response, continued treatment can maintain a high level of sustained HBV DNA suppression, and the rate of resistance to entecavir is low, with a five-year incidence of resistance of about 1.2%. (4) Tebivudine: It is also potent in suppressing the virus, and its overall efficacy and incidence of drug resistance is better than that of the lamivudine group. The overall incidence of adverse events was similar to that of lamivudine, but the incidence of grade 3-4 creatine kinase (CK) elevation was 7.5% and 12.9% at 52 and 104 weeks of treatment, respectively, which was higher than that of 3.1% and 4.1% in the lamivudine group. (5) Tenofovir: Tenofovir is structurally similar to adefovir, but with less nephrotoxicity and a therapeutic dose of 300 mg per day, and no resistance variants have been found. This drug has not been approved for marketing in China. 2. Issues related to nucleoside (acid) drug therapy Baseline testing of relevant indicators before treatment: (1) biochemical indicators: mainly ALT, AST, bilirubin and albumin; (2) virological markers: mainly HBV DNA and HBeAg, anti-HBe; (3) routine blood tests, serum creatinine and CK, etc. according to the needs of the disease. If conditions allow, liver histopathological examination should be performed before and after treatment. (2) Virological markers: mainly HBV DNA, HBeAg and anti-HBe, which should be tested once every 1 to 3 months after the start of treatment and once every 3 to 6 months thereafter; (3) Regular blood tests, serum creatinine and CK according to the needs of the disease. (3) according to the needs of the disease, regular testing of blood routine, serum creatinine and CK and other indicators.