The incidence of liver damage during antituberculosis treatment in HBsAg-positive TB patients was 57.5%, while only 10.0% of HBsAg-negative TB patients developed liver function abnormalities, data suggesting that HBsAg-positive TB patients tolerate poorly to intensive antituberculosis chemotherapy drugs. Studies have shown that the mechanism of hepatic damage caused by antituberculosis drugs may be: 1. The cytotoxicity of the drug directly damages hepatocytes, leading to hepatocyte necrosis, such as the drug hepatitis that can be caused by isoniazid. 2. The drug itself and its metabolites interfere with or block an important metabolic pathway or bile excretion function of hepatocytes, indirectly causing hepatocyte damage: for example, rifampin and pyrazinamide can cause hepatocyte degeneration and necrosis. 3, the original liver disease, drug metabolism abnormalities, affecting the metabolism and clearance of drugs. 4, drug interactions can affect the metabolic process of drugs due to competition for the action sites of liver microsomal enzymes. When liver damage occurs during anti-tuberculosis treatment, if only a slight increase in transaminases generally do not stop the drug, because stopping the drug may increase the resistance of Mycobacterium bovis. To reduce liver damage and ensure that TB patients successfully complete chemotherapy, patients’ liver function and hepatitis B surface markers should be carefully checked before antituberculosis treatment, and liver function should be monitored regularly during antituberculosis treatment; for HBsAg-positive patients, it has been suggested that antiviral and hepatoprotective therapy should be routinely given, and for patients in the stage of viral replication or with abnormal liver function, combined anti-hepatitis B virus therapy (lamivudine or Adefovir).