With the improvement of people’s living standard and the decrease of sports activities, there are more and more people with dyslipidemia, and high lipid level is also an important cause of hypertension, so lipid-regulating drugs are very necessary in the treatment of hypertension. Many patients do not know much about the damage of lipid-lowering drugs on liver function, so the author will give you a popularization according to his knowledge. First, the classification of lipid-lowering drugs The current clinical drugs used to regulate dyslipidemia can be divided into four categories. The first category is statins, including simvastatin (Sulforaphane), pravastatin (Praglum), lovastatin (Meldonium), fluvastatin (Lysine), atorvastatin (Ala). In addition, there are also some proprietary Chinese medicines containing statin ingredients, such as Blood Lipid Kang. Statins are the most widely used class of lipid-lowering drugs with the largest dosage worldwide, and are suitable for patients with mainly high cholesterol. The second category is fibrates, including gemfibrozil (Norfibrozil), fenofibrate (Lipin), and benzofibrate (Bifid), which are suitable for patients with mainly high triglycerides. The third category is niacin, which is mainly used for the treatment of patients with simple triglyceride elevation, as well as those with predominantly elevated serum triglycerides and mildly elevated serum total cholesterol. Commonly used drugs include niacin, nicotinic acid inositol ester, acipimox (Lupin), etc. The fourth category is bile acid chelators, which are suitable for people with simple increase in total serum cholesterol. Commonly used drugs include clofentezine, clofentezine and glucosamine (lipid-lowering 3 resin). Second, the degree of liver damage varies Lipid-lowering drugs need to be taken for a long time, and all have side effects, so the side effects and their hazards should be closely monitored in the process of medication. Statins are the most widely used lipid-regulating drugs with the largest dosage in the world. They are safe for long-term use, but they can cause dose-dependent and asymptomatic elevation of serum aminotransferases. The probability of statin causing transaminases greater than 3 times the upper limit of normal value is 0.5%-2.0%, and a reduction in dosage can often lower transaminases. Patients with underlying liver disease (including fatty liver) who take statins and whose transaminases are elevated less than two times the upper limit of normal values are generally not affected by treatment. Those with significant elevations should have their dosage reduced or discontinued. Transaminases usually return to normal within 2 to 3 months after discontinuation. Active liver disease and hypersensitivity to this drug are contraindicated. Liver enzyme increases usually occur within 16 weeks of dosing and therefore liver function tests should be performed prior to treatment, at 4 and 12 weeks of treatment, or after increasing the drug dose. There is no conclusive evidence to date that statins exacerbate liver injury in patients with viral hepatitis, alcoholic liver disease, or primary biliary cirrhosis, and no change in statin dose is generally necessary for these liver diseases that are complicated during lipid-modifying therapy. Clofibrate, a beta-lipid-lowering drug, has a high probability of causing abnormal serum aminotransferases, with moderate elevation of aminotransferases in 10% of cases, and occasionally granulomatous hepatitis and cholestatic jaundice. Fenofibrate can cause elevated transaminases in up to 20% of cases, with a few manifestations of cholestatic hepatitis and chronic hepatitis. In contrast, there is little evidence that gemfibrozil causes liver damage. Niacin analogs have the highest rate of liver function abnormalities, up to 30%. Jaundice may develop in 3% of patients who take 3 g daily for more than 1 year. Extended-release dosage forms such as aluminum niacin are more likely to cause liver damage and to cause jaundice earlier than short-acting niacin preparations, and a few patients may develop cholestasis and acute liver failure. The liver damage of the above three types of drugs is objective, and there are clear precautions in the instructions of each drug. Patients should pay attention to the following aspects when using these drugs: 1. A treatment plan must be formulated and drugs selected by a doctor after examination and diagnosis of hyperlipidemia. 2. Liver function should be tested regularly before and during the course of medication. 3. After a period of treatment, patients should go to the hospital regularly to review and let the physician decide whether to adjust the medication and dosage, do not purchase the medication and increase the dosage at will. 4. During the treatment period, if other diseases appear and require drug treatment, a physician or pharmacist should be consulted to avoid serious adverse reactions caused by the combined use of drugs. Therefore, the use of lipid-lowering drugs is not arbitrary, and we must pay attention to their damage to the liver to avoid second damage to the body.