Fat milk is a preparation made from soybeans emulsified with a certain amount of phosphatidylcholine (lecithin), and is mainly used clinically to supplement patients with appropriate calories and essential fatty acids. The common adverse effects of fatty milk include fever and nausea, allergic reactions and anaphylaxis, liver function impairment, abnormal penile erection, diffuse intravascular coagulation, pulmonary artery embolism, etc. Our department used adenosylmethionine combined with magnesium isoglycyrrhizate to treat a case of cholestatic liver damage caused by the use of fatty milk after pancreaticoduodenal surgery, which is reported as follows: 1. Medical history The patient was a male, 70 years old, admitted to the hospital due to skin sclera yellow staining with urine days, and was in good health. After admission, liver function was checked: total bilirubin (TBIL) 165.7umol/L, direct bilirubin (DBIL) 115.2umol/L, indirect bilirubin (IBIL) 50.5umol/L, alkaline phosphatase (ALP) 394U/L, glutamine transpeptidase (GGT) 230U/L, alanine transaminase (ALT) 75U/L, glutathione The abdominal CT examination suggested an occupying lesion in the head of the pancreas and pancreatic head cancer. The diagnosis of pancreatic head cancer was confirmed by gastroscopic puncture and biopsy of the pancreatic head mass for pathological examination. The decision was made to perform pancreaticoduodenectomy and postoperative intravenous nutritional support treatment with glucose, amino acids and fatty milk and liver protection treatment with glutathione. On the first postoperative day, TBIL 220.5umol/L, DBIL 160.2umol/L, IBIL 60.3umol/L, ALP 187U/L, GGT 40U/L, ALT 229U/L, AST 862U/L were rechecked, and intravenous nutritional support therapy including fat milk was continued. TBIL282umol/L, DBIL250umol/L, IBIL32.5umol/L, ALP180.7U/L, GGT32.6U/L, ALT254U/L, AST602U/L were rechecked on day 2. fat emulsion was stopped on day 3, dexamethasone 10mg ivdrip was used once, glutathione was stopped and adenosine was used instead Methionine 1g ivdrip qd + magnesium isoglycyrrhizate 150mg ivdrip qd treatment. TBIL 210.2umol/L, DBIL 170.2umol/L, IBIL 40.4umol/L, ALP 160.7U/L, GGT 27U/L, ALT 168U/L, AST 337U/L were rechecked. on the fourth postoperative day, we switched to intravenous nutritional support with three liter bags of Carvin (containing 20% fat milk 255ml) and checked TBIL335.4umol/L, DBIL239.7umol/L, IBIL95.7umol/L. After the fifth day, the intravenous infusion containing fat milk was stopped and TBIL383.6umol/L, DBIL256.8umol/L, IBIL126.8umol/L were checked. The patient recovered well and was discharged with oral hepatoprotective drugs. Discharged from hospital. (2) The first symptoms may include fever, rash, itching and other allergic phenomena; (3) eosinophils in the peripheral blood >6%; (4) clinical and pathological signs such as intrahepatic cholestasis or parenchymal cell damage; (5) clinical and pathological signs such as intrahepatic cholestasis or parenchymal cell damage; (6) the patient’s liver was damaged by the drug. (5) positive lymphocyte transformation test or macrophage movement inhibition test; (6) negative hepatitis viral markers such as HBsAg, anti-HBc, anti-HAVIgM, anti-HCV, anti-HDV, anti-HEV, etc.; (7) occasional re-dosing followed by liver damage. The diagnosis of drug-related liver disease can be made by having any 2 of the above (1), plus (2)-(7). The patient was treated with fat emulsion for intravenous nutritional support after surgery, and the bilirubin increased sharply after using fat emulsion. After stopping the fat emulsion and treating with hormone and intensive hepatoprotective drugs, the bilirubin decreased, and after using fat emulsion containing nutritional solution again, the liver function deteriorated again and the bilirubin increased progressively. In pharmacological liver damage, adenosylmethionine shows abnormal metabolism, reduced hepatic synthesis and supply, impaired transmethylation and transmercaptation, causing decreased hepatocyte membrane fluidity and reduced bile secretion, resulting in accumulation of substances excreted via bile in the blood, with clinical manifestations of a series of syndromes and abnormal liver function adenosylmethionine, as the main methyl donor of human cells, plays an important role in phospholipid synthesis. It regulates the fluidity of hepatocyte membrane by methylation of cytoplasmic membrane phospholipids and facilitates the excretion of bile. Adenosylmethionine is a dependent substance in the synthesis and operation of glutathione, and plays an important role in the stability of glutathione, thus improving the detoxification function of hepatocytes. As long as the bioavailability of adenosylmethionine in the liver is within the normal range, it can help to improve bilirubin metabolism in the liver, relieve biliary stasis and reduce jaundice and liver function damage in patients. Magnesium isoglycyrrhizate is extracted from the natural plant licorice and refined by alkali-catalyzed isomerization into salt. Pharmacological experiments have proved that magnesium isoglycyrrhizate has a significant effect on the elevation of serum ALT and AST caused by carbon tetrachloride, D-aminogalactose and thioacetamide, and also can significantly reduce the morphological damage of D-aminogalactose to the liver and improve the chronic damage of immune factors to the liver morphology. Magnesium isoglycyrrhizate has strong anti-inflammatory effects on protecting hepatocytes and improving liver function. Adenosylmethionine and magnesium isoglycyrrhizate have been reported clinically for the treatment of drug-induced liver damage, but the combination of the two has not been reported for the treatment of drug-induced cholestatic liver disease. Some scholars reported that the combination of adenosine methionine and magnesium isoglycyrrhizate in 30 cases of drug-related cholestatic liver disease had a synergistic effect, and the total effective rate could reach 90%. The combination of adenosine methionine and magnesium isoglycyrrhizate in the early stage of treatment of drug-related cholestatic liver disease can shorten the course of the disease and reduce the chronic and lasting damage to the liver. The above is for the reference of clinical colleagues and patients.