I. How to understand hepatitis B virus carriers? Chronic hepatitis B virus infection goes through four stages: immune tolerance period, immune activation period, immune control period and immune reactivation period. The difference between the immune tolerance phase and the immune activation phase is that the former is characterized by high serum viral load, normal transaminase levels and no significant inflammation and fibrosis in the liver, while the latter is characterized by high serum viral load, elevated transaminase levels and significant inflammation and fibrosis in the liver. Immunocontrol and immunoreactivation phases manifest as “minor triplets”; the difference is that the former manifests with low serum viral load, normal transaminase levels, and no significant liver inflammation and fibrosis, while the latter manifests with high serum viral load, elevated transaminase levels, and significant liver inflammation and fibrosis. ”High, medium and low viral loads are usually defined as serum hepatitis B viral nucleic acid concentrations greater than 10^7, 10^7 to 10^7, and 10^7 to 10^7, respectively. High, medium and low viral loads usually refer to serum hepatitis B viral nucleic acid concentrations greater than 10^7, 10^7-10^4, and less than 40 international units per milliliter, respectively; normal transaminase levels generally refer to serum alanine transaminase less than 40 international units per milliliter. Broadly speaking, hepatitis B carriers should be all people with chronic hepatitis B virus infection, regardless of the stage of the virus infection. A narrowly defined hepatitis B carrier is a person with chronic hepatitis B virus infection who is in the immune tolerance and immune control periods. Most physicians understand hepatitis B virus carriers in the narrow sense. Clinical experience and research have concluded that hepatitis in the narrow sense of hepatitis B carriers is in a relatively quiescent state and does not require pharmacological intervention, but must be under strict medical observation. The hepatitis B virus carriers mentioned in this article refer to hepatitis B virus carriers in the narrow sense. Second, how to understand liver function indicators? The function of the liver is extremely complex and has an extremely strong compensatory capacity; the assessment of liver function is also extremely difficult. The vast majority of patients with cirrhosis are able to meet the needs of life to varying degrees. The ultimate cause of death in patients with cirrhosis is usually the adverse events associated with the portal hypertension that accompanies cirrhosis, such as upper gastrointestinal bleeding, hepatic encephalopathy, hepatopulmonary syndrome, and hepatorenal syndrome. Liver function tests currently in clinical use cover only a few indicators of liver injury, liver function and portal hypertension, and are laboratory packages to screen for the presence or absence of liver disease based on the limited understanding of liver function in recent medicine. The contents of liver function packages are not standardized in different foreign and domestic medical institutions, and most include alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, ? -Glutamyl transpeptidase, conjugated bilirubin, total bilirubin, albumin, globulin, etc. In the past 20 years, many medical institutions have included cholinesterase and total bile acids in the package. Third, how to monitor liver function in hepatitis B virus carriers? The frequency of monitoring should be different for different types of hepatitis B virus carriers. The frequency of liver function monitoring for hepatitis B virus carriers with “major triple yang” is usually once every 3 to 6 months. Patients in the immune tolerance phase do not experience significant liver damage, the liver is in good underlying condition, and the liver damage caused by the initial immune activation is not significant; patients entering the immune activation phase usually show persistent or progressive hepatitis activity. Therefore, significant hepatitis activity within a period of 3-6 months rarely results in a life-threatening disease state, and non-significant hepatitis activity within a period of 3-6 months is rarely missed. The frequency of liver function monitoring for “small triple-positive” hepatitis B carriers is usually once every 3 months. Patients in the immune control phase have experienced significant liver damage, at least in part, and a few of them may have cirrhosis, a relatively poor underlying condition of the liver, and liver damage caused by re-occurring immune activation, whether severe or not, may lead to a life-threatening disease state; patients entering the immune reactivation phase show transient or persistent hepatitis activity. Therefore, hepatitis B carriers with “minor triplets” should have their liver function monitored more frequently than those with “major triplets”. The content of monitoring should be different for different types of hepatitis B carriers. The monitoring of liver function in “major triple positive” hepatitis B carriers can be simplified by testing alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, alkaline phosphatase, alkaline phosphatase, alkaline phosphatase and alkaline phosphatase. -Glutamyl transpeptidase, conjugated bilirubin, total bilirubin, albumin, globulin, etc. can generally detect hepatitis activity and roughly determine the severity of hepatitis activity. It is best to monitor the liver function of hepatitis B carriers with “minor triple positive” and to monitor cholinesterase and total bile acids at the same time. Although transaminases are an indicator of early liver damage, not all patients, especially those with cirrhosis, have elevated transaminases. Total bile acids are an important alternative indicator for detecting early liver damage; cholinesterase reflects liver reserve function with greater sensitivity than albumin. The usual liver function package has limited ability to detect hepatitis activity because liver function-related indicators are only the “fruit” of liver injury and do not reflect the “cause” of liver injury. The immunological mechanisms underlying the development of hepatitis activity in chronic hepatitis B virus infection have not been elucidated. However, one of the virological manifestations of immune activation or reactivation is a significant decrease in serum viral load. Patients with early immune activation will have a shift from high to moderate serum viral load; if immune activation is significant, their serum viral load will shift from high to low. Conversely, patients with immune reactivation will have a low to moderate serum viral load; if immune activation is significant, the serum viral load will go from low to high. The usual liver function package has a limited ability to detect cirrhosis due to the strong reserve function and compensatory capacity of the liver. In fact, clinically non-significant portal hypertension or occult portal hypertension has already occurred in pre-cirrhosis. Platelet count in routine blood tests is an important indicator for detecting cirrhosis, with higher sensitivity and specificity than the relevant indicators in the usual liver function package. Therefore, it is better to monitor liver function package and blood routine simultaneously for hepatitis B virus carriers with “small triple yang”. What are the misconceptions of liver function monitoring for hepatitis B virus carriers? The assessment of liver function and liver disease status is subject to great uncertainty, at least because of the different underlying liver conditions and hepatitis activity in different patients, the coexistence of liver damage and repair, innate differences in each index and different plasma half-lives, etc. Therefore, the determination of liver disease status needs to follow the principle of integration and complementarity. One of the misconceptions of liver function monitoring is to replace the efficacy of the liver function package with one of the indicators in the liver function package. For example, to represent the degree of liver injury by the degree of transaminase elevation: transaminase is only an indicator of liver injury, and although it can reflect the degree of liver injury to a certain extent, its elevation does not parallel the degree of liver injury; to represent the liver reserve function by bilirubin elevation: there are many factors that affect bilirubin metabolism. Hepatocellular injury, bile duct injury and obstruction, and individual differences in bilirubin metabolism all affect the degree of bilirubin elevation. The second misconception about liver function monitoring is that it emphasizes the role of the liver function package and ignores the value of other related indicators. The name of the liver function package itself is a misunderstanding. Virological indicators outside the liver function package, serum virological markers and viral load, coagulation indicators, immunological indicators such as immunoglobulins, etc. also have some discriminatory efficacy on the degree of liver damage and liver reserve function. The third misconception about liver function monitoring is that all hepatitis B carriers should be monitored with the same frequency and content. The frequency and content of monitoring should be different for different types of hepatitis B carriers because of the differences in liver underlying conditions and hepatitis activity between “major triple-positive” and “minor triple-positive” carriers.