Drug-related liver injury is one of the most common and serious adverse reactions in the course of regular chemotherapy for tuberculosis. According to statistics, 10%-30% of TB chemotherapy patients can develop liver injury, accounting for 8%-13% of all drug-related liver injury. The mechanism of hepatotoxicity of anti-tuberculosis drugs is still not fully understood, and anti-tuberculosis drugs can be divided into two categories based on the predictability of drug-generated liver disorders: those with a close quantitative-activity relationship and those with a less close quantitative-activity relationship. The occurrence of liver damage caused by antituberculosis drugs is closely related to the dose of the drug, such as isoniazid, rifampin, pyrazinamide, aminothiourea, ethanethionamide, and prothiouracil. The hepatocellular toxicity of these drugs is mainly direct damage and indirect damage from the toxic effects of the drugs themselves or their metabolites. The direct damage is the hepatocyte toxicity of the drug or its metabolites directly causing hepatocyte necrosis and fat deformation, for example, isoniazid combines with acetyl group to form acetylated isoniazid through the action of N2 acetyltransferase in the liver, and then acetylated isoniazid is hydrolyzed to the more toxic acetylhydrazine in the liver, and the latter is transformed into reactive intermediate through microsomal enzymes in the hepatocytes. The latter is transformed into reactive intermediate by microsomal enzymes in hepatocytes, which then binds to cellular proteins leading to hepatocyte deformation and necrosis. The metabolic process generates low-molecular free radicals, which can also induce lipid peroxidation and cause drug-related hepatitis. Indirect damage is the metabolites and their proprieties interfere with or block the hepatocytes and an important metabolic pathway or bile excretion function, thus causing damage to hepatocytes or bile excretion disorder, such as pyrazinamide by affecting protein synthesis and other links to the hepatocyte cytoplasmic membrane or sub-micro organelles damage, resulting in the loss of cell integrity, and then hepatocyte degeneration and necrosis. Rifampicin is a large molecule drug that is excreted mainly in the bile, and its concentration in the bile can be 2,000 times that of plasma. It mainly interferes with the binding and excretion of bilirubin and glucuronide, resulting in increased unconjugated bilirubin, jaundice, and impaired excretion of pigment. Among the drug interactions should not be ignored, drug metabolism in the liver usually goes through two steps, the first step includes oxidation, reduction or hydrolysis process; the second step is the binding process, the binding reaction includes at least four main chemical effects, namely glucuronidation, sulfation, glutathione binding and acetylation, isoniazid, rifampicin, p-aminosalicylate sodium metabolism in the liver all need acetyltransferase, metabolism to form Amide compounds, there may be enzymatic competition between them, such as sodium p-aminosalicylate can reduce the rate of isoniazid acetylation and increase isoniazid hepatotoxicity. Rifampicin is a liver microsomal enzyme inducer, which can increase its activity, accelerate isoniazid metabolism and increase isoniazid toxicity. The dose-effect relationship is not close (so-called allergic type): that is, the occurrence of liver damage caused by anti-tuberculosis drugs is not closely related to the dosage of drugs. This type is mainly drug allergy and idiosyncratic reaction. Liver damage caused by small doses of isoniazid, pyrazinamide, and rifampicin has also been reported. On liver biopsy, eosinophil infiltration or granuloma formation in the confluent area and lobules is seen, and intrahepatic cholestasis, such as bile emboli, is seen. Immunological studies of intrahepatic cholestasis suggest that drug-induced intrahepatic cholestasis is induced by immunological mechanisms. The active factor is a lymphatic factor, named cholestatic factor, which has been confirmed by liver biopsies and is involved in immune liver injury and can impair the structure of bile excretion containing microfilaments. Most scholars believe that the liver damage caused by sodium p-aminosalicylate is allergic, because jaundice and liver damage caused by sodium p-aminosalicylate often appear after high fever and rash, and are accompanied by a variety of allergic reactions such as allergic pulmonary infiltrates and arthralgia, because sodium p-aminosalicylate may bind to carrier proteins and become antigens, causing cellular immune reactions that damage the liver. Rifampicin can cause various types of hypersensitivity reactions. In intermittent, high-dose cases, most of the rifampicin antibodies can be detected in the serum, and the symptoms are drug rash, urticaria, eosinophilia, etc. Type IV hypersensitivity reactions can lead to hepatocellular damage. Risk factors for severe liver injury from antituberculosis drugs include advanced age, alcoholism, poor nutrition, genetic factors, individual differences, immune status, HBV carriage, and previous history of liver disease. Most of the patients with liver injury are asymptomatic, but abnormalities are found during liver function tests. A few patients may show typical manifestations of hepatitis, such as nausea, aversion to oil, weakness, jaundice, liver enlargement, and pain in the liver area. In case of mild liver damage caused by anti-tuberculosis drugs, anti-tuberculosis drugs can be stopped and liver-protective drugs can be added to the treatment, and liver function can generally be restored to normal. The incidence of moderate reversible aminotransferase elevation is about 15%-30% when anti-tuberculosis drugs cause moderate liver injury, and discontinuation of drugs may increase mycobacterial resistance. Anti-tuberculosis drugs cause severe liver injury, the need to promptly discontinue anti-tuberculosis drugs, otherwise it can lead to irreversible liver damage. If liver injury is accompanied by persistent nausea, vomiting, weakness and jaundice, the drug should be discontinued. If liver injury is accompanied by systemic metabolic reactions such as fever, rash, arthritis and increased eosinophils, it is likely to be allergic liver injury and should be discontinued immediately. It should be noted that there is no definite relationship between the degree of transaminase elevation and the severity of hepatotoxic reactions, and a mild liver injury may become the first manifestation of a serious liver injury. Therefore, discontinuation of antituberculosis drug therapy often depends on the clinical experience of the physician and the clinical presentation of the patient. If the drug causing liver injury is identified, the drug should no longer be used. If necessary, the chemotherapy regimen needs to be adjusted. Second-line antituberculosis drugs with less hepatotoxicity, such as quinolones, sodium para-aminosalicylate, and bupropion, may be used instead. Next, hepatic support therapy should be given. Patients should be given bed rest, supplemented with glucose, B vitamins, clear protein, inosine, and vitamin K, blood or plasma transfusion for those with bleeding tendency. Ensure sufficient calories, maintain water, electrolyte and acid-base balance, and keep the internal environment stable. For high aminotransferase, lower enzyme treatment, such as potassium magnesium menthylate, hepatocyte, Kessler, cilipramine, bifenesin, glycine, reduced glutathione, and hepatocyte growth promoter can be given. Prevention is also important. Before treatment, the patient should be asked in detail whether there is a history of hepatitis and other conditions that may affect liver function. Liver function should be checked diligently during treatment, and for high-risk patients, liver function can be rechecked in 1 to 2 weeks, and anti-tuberculosis drugs with low hepatotoxicity or appropriate dose reduction should be used as much as possible. Some studies have shown that routine addition of hepatoprotective drugs can reduce the incidence of liver injury in high-risk patients. In addition, reasonable rest and active improvement of the patient’s nutritional status are also important. In conclusion, patients with risk factors should be well treated with early hepatoprotective therapy and be alert to the occurrence of liver injury. Timely, reasonable and effective treatment after the occurrence of drug-related liver injury can ensure that patients successfully complete the anti-tuberculosis course.