Almost all cyclooxygenase inhibitors are associated with liver damage, and the risk of liver disease in patients taking cyclooxygenase inhibitors is two to three times greater than in patients without such drugs. Transaminases are elevated in mild cases and hepatocellular necrosis in severe cases, but most hepatotoxicity manifests itself as a mild increase in liver enzyme levels, and hepatic damage with overt clinical symptoms is very rare. Most cyclooxygenase inhibitor liver damage is a specific somatic reaction, drug-induced hypersensitivity reaction or individual metabolism of the drug is abnormal, which is characterized by a low incidence, dose-independent, latent period of weeks to months, and difficult to predict its occurrence. Acetaminophen is metabolized by hepatic cytochrome P450 oxidase, which produces excessive active metabolite N-acetyl-p-benzoquinone imine, such as long-term high-dose use of acetaminophen can lead to acute toxic hepatic necrosis, and in severe cases, it can lead to coma or even death; use with caution in children under the age of 3. Domestic acetaminophen-containing combination preparations amount to more than 30 kinds, and its over-the-counter drugs are sold in large quantities and widely used, therefore, it is not recommended to use it for the treatment of liver disease caused by acetaminophen. Acetaminophen-induced liver damage should be highly emphasized. Large doses of POTAMINOPHEN can cause liver damage, producing jaundice and hepatitis. Salicylates can cause liver damage in atopic patients. Fever caused by viral infections in children (e.g., influenza B virus) can develop steatosis and hepatic encephalopathy complications are a common cause of death when aspirin is used, so aspirin is not recommended for children. Most liver damage due to cyclooxygenase inhibitors improves within a few days to weeks after prompt discontinuation of the drug.