In recent years, the incidence of malignant tumors has been increasing year by year, and the mortality rate has ranked first in the overall causes of death. Chemotherapy occupies an important position in the treatment of malignant tumors, and with the continuous development of anti-tumor drugs, the prognosis of malignant tumors has been significantly improved. However, the adverse reactions caused by antineoplastic drugs bring new problems for tumor treatment. Drug-related liver damage is a common adverse reaction during oncology treatment, especially in China where the incidence of hepatitis is high, and hepatotoxicity and treatment strategies for oncology patients with underlying liver disease deserve attention. Evaluation of liver function Indicators commonly used to detect liver function in clinical practice include transaminases, bilirubin, alkaline phosphatase, serum albumin and clotting time [1]. These indicators objectively reflect the activity of the liver from different aspects. A comprehensive understanding of the significance of each index can help to correctly assess liver function. Transaminases: a sensitive reflection of the destruction of hepatocytes. The most commonly tested in clinical practice are alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Normal concentrations of serum ALT and AST are usually less than 30-40 IU/L. The highest concentrations of ALT are found in the liver, and the highest to lowest concentrations of AST are found in the liver, heart muscle, and skeletal muscle, in that order. For liver disease, ALT is more specific. Serum aminotransferases can be pseudoincreased or decreased in some cases. Some drugs can cause pseudoincreases in aminotransferases and renal failure can cause pseudoincreases in AST (not ALT). Most liver lesions result in elevated transaminases, but transaminase measurements are not proportional to the degree of hepatocyte necrosis. Alkaline phosphatases (ALP): a group of enzymes that catalyze the hydrolysis of organophosphate esters. Distributed in several organs, serum alkaline phosphatase is mainly derived from the liver, bone and intestine. Elevated ALP may be caused by hepatocyte destruction resulting in release into the bloodstream or by biliary stasis preventing the secretion and excretion of ALP produced by various organs. ALP is elevated to more than four times the upper limit of normal in approximately 75% of patients with biliary sludge; a variety of liver diseases may cause ALP to be elevated to three times the level, and such elevations lack specificity and are sometimes seen in other diseases without liver involvement; elevated ALP alone or incompatible with elevated transaminases is seen in partial biliary obstruction due to gallstones or tumors, early stages of biliary liver disease, and extrahepatic disease. Bilirubin: reflects the ability of the liver to remove endogenous and exogenous substances from the blood circulation. The high reserve capacity of the liver to remove bilirubin makes this indicator less sensitive and sometimes not even elevated in cases of moderate to severe liver parenchymal injury and partial or transient biliary obstruction. Albumin and clotting time: reflect the synthetic capacity of the liver. Drug-related liver damage In 1989, the International Consensus Conference of European and American experts in Paris reached a consensus on drug-related liver damage (Paris Consensus), defining liver damage as an increase in serum ALT or conjugated bilirubin levels more than twice the upper limit of normal, or an increase in AST, ALP and total bilirubin levels, one of which is more than twice the upper limit of normal. The conference also pointed out that the diagnosis of liver damage by other biochemical indicators is non-specific; while the increase of the above indicators within 2 times of the upper limit of normal value is called “abnormal liver function test”, but should not be called “liver damage”. Antitumor drugs and liver damage: Most antitumor drugs are metabolized by liver and kidney, so liver toxicity is more common. Antineoplastic drugs may cause liver damage in three ways: direct damage to hepatocytes; aggravation of underlying liver disease, especially viral hepatitis; alteration of the metabolism and secretion of antineoplastic drugs due to underlying liver disease, which prolongs the duration of drug action in the body and increases chemotherapy toxicity. Direct damage to hepatocytes: mostly idiosyncratic, dose-independent and unpredictable. Clinical manifestations are diverse and can range from asymptomatic biochemical abnormalities to acute jaundice [2]. Pathology can manifest as chronic inflammatory changes, endothelial damage or thrombosis (e.g. veno-occlusive disease VOD). The prognosis of liver damage caused by antineoplastic drugs varies widely, with some drugs having reversible hepatotoxicity and others causing fibrosis or cirrhosis even after drug discontinuation. The presence of underlying liver disease such as hepatobiliary system tumors, viral hepatitis, and malnutrition increases the likelihood of liver damage caused by antineoplastic drugs. Aggravating liver underlying disease: In tumor patients with liver underlying disease, chemotherapy may aggravate liver disease and also increase the risk of liver damage from chemotherapeutic drugs. To mitigate the adverse effects of chemotherapy, concurrent treatment of liver underlying disease is recommended. Some chemotherapeutic drugs should be avoided and some chemotherapeutic drugs should be reduced in patients with severe liver disease. Common underlying liver diseases are hepatitis B and C infection; chemotherapy can activate hepatitis B virus replication, and prophylactic lamivudine is recommended for hepatitis B patients to reduce viral activation; it is unclear whether chemotherapeutic agents activate hepatitis C virus replication, and the incidence of VOD appears to be increased in hepatitis C patients receiving high-dose chemotherapy or stem cell transplantation. Altered drug metabolism: Liver insufficiency can affect the metabolism of certain chemotherapeutic drugs, resulting in increased drug concentration or prolonged duration of action and increased drug toxicity. For patients with tumor liver metastases, it is generally recommended that the first chemotherapy should be appropriately reduced, and if the liver metastases respond to chemotherapy, the subsequent chemotherapy can be further increased in dose. Diagnosis of liver damage by antineoplastic drugs: The diagnosis of liver damage by antineoplastic drugs is difficult. Generally, drug-related liver damage is considered more likely when the following conditions are met: no underlying disease before chemotherapy, clinical symptoms or blood biochemical abnormalities after chemotherapy, improvement of liver damage after stopping the drug, and more rapid and severe appearance of liver damage after re-dosing. The differential diagnosis includes tumor progression, coexisting underlying liver disease, and liver damage caused by other drugs. Treatment of liver damage caused by anti-tumor drugs: The first treatment of liver damage caused by anti-tumor drugs is to stop the drugs, and this is to use liver-protective drugs. At present, there are many kinds of hepatoprotective drugs, which can be divided into the following categories according to the mechanism of action: a. Anti-inflammatory and hepatoprotective drugs: they can scavenge free radicals, inhibit the covalent binding of free radicals with hepatocyte membrane, antioxidant, protect hepatocyte membrane; resist mitochondrial damage, maintain the stability of mitochondrial membrane; resist hepatocyte nuclear DNA degradation, inhibit the release of cytochrome C, which initiates apoptosis signal, reduce the level of TNFa, etc. to prevent normal hepatocyte apoptosis; inhibit the expression of TGF-β, anti-liver fibrosis; have certain immunomodulatory effects; may make infected virus hepatocytes apoptosis by inducing. Including glycyrrhizin class: heparin, Mennen; silymarin class: ligaron, cilibinan; pentosidine class: dicyclomine (Baxenol), biphenyldiamine, liver protection tablets. Second, cell repair class: a physiological phospholipid, which is consistent with endogenous phospholipid in chemical structure, restores damaged liver function and enzyme activity to normal; regulates the energy balance of the liver; promotes liver tissue regeneration. Representative drugs include: Ezinfluenza, liver health, etc. Third, detoxification and liver protection class: it can combine with various chemical substances and their metabolites, scavenging oxygen ions and free radicals in the body through its sulfhydryl group, increasing antioxidant function; maintaining the concentration of glutathione in blood and liver cells, inhibiting the formation of mitochondrial peroxidized liposomes; increasing the content of intracellular ATP, protecting liver cell membranes, promoting liver enzyme activity and increasing liver detoxification function; in the body Promote hepatocyte regeneration by participating in the synthesis of purine nucleotides. Representative drugs include: glutathione (atomolane), thiopronine (Kesilai), glucuronide (hepatolide), penicillamine, etc. Cholestatic and hepatoprotective drugs: promote the secretion of endogenous bile acids and inhibit their reabsorption; antagonize the cytotoxic effect of hydrophobic bile acids and protect hepatocytes; immunomodulatory effect and inhibit the abnormally enhanced immune response. Representative drugs include: adenosylmethionine (Stamet), ursodeoxycholic acid, gardenia jasminoides, bitter yellow injection. Chinese herbal medicine: Yin Chen, Weeping grass, etc. Sixth, vitamins and coenzymes: various water-soluble vitamins, such as vitamin C, vitamin B complex and coenzyme A, etc. Principles for determining liver damage caused by antineoplastic drugs: Be alert to the possibility of drug-related liver damage when the following conditions occur: ALT > 2-3 times the normal high limit or ALP > 1.25 times the normal high limit or TBil > 1.5 times the normal high limit, one of which should be rechecked after 1 week. Consider discontinuing the drug when one of the following conditions occurs: ALT > 3-5 times the normal high limit or ALP > 1.5 times the normal high limit or TBil > 2 times the normal high limit. Once antineoplastic drug-induced liver damage occurs, treatment [5]: (1) mainly discontinuation or dose reduction, and the next treatment strategy should be decided according to the degree of liver damage. (2) N-acetylcysteine: a reducing sulfhydryl group, which directly captures unpaired electrons and acts as an antioxidant; replenishes endogenous cellular GSH and enhances cellular detoxification; improves the mitochondrial tricarboxylic acid cycle and improves the function of hepatocytes; inhibits the activation of NF-kB and reduces NO damage. In clinical trials of paracetamol-induced liver damage, it was proved to be effective against drug-induced liver damage. (3) Corticosteroids: have a role in the treatment of liver damage caused by hypersensitivity reactions, but there is a lack of sufficient evidence of efficacy in most other liver damage. Most patients’ liver function can be normalized after stopping the drug. In conclusion, there is a lack of specific drugs for antineoplastic drug-induced liver damage. Prognosis of antineoplastic drug-induced liver damage: Patients who develop jaundice have a poor prognosis; patients who develop acute liver failure and are not transplanted can have a mortality rate of 80% or more.