The main components of cell membranes include phospholipids and cholesterol. Changes in lipid metabolism will affect their synthesis, thereby affecting cell proliferation; a variety of lipid molecules are involved in various cell signal transduction, inflammation and vascular regulation processes. Abnormal lipid metabolism is closely related to tumor occurrence, development, invasion and metastasis.
Tumor cells exhibit uncontrolled de novo fatty acid synthesis and enhanced lipid synthesis, providing a corresponding microenvironment for the continuous proliferation of tumor cells. The lipid metabolism of tumor hosts is relatively complex. When lipid metabolism and synthesis are abnormal, there may be different degrees of exogenous lipid utilization disorders, which induce dyslipidemia in tumor patients.
The main changes of lipid metabolism in tumor patients are enhanced adipose tissue decomposition and mobilization, decreased exogenous lipid utilization, plasma lipoprotein chylomicrons, very low density lipoprotein (VLDL) and elevated triglycerides (TG). Long-term abnormal lipid metabolism induces the depletion of stored fat in tumor patients, and even the breakdown of skeletal muscle protein, which leads to the decrease of lean muscle mass in patients, and induces or aggravates cancer cachexia. Correcting abnormal blood lipids in tumor patients can alleviate the occurrence of cachexia to a certain extent. 01—Evidence-based medical evidence, hyperlipidemia may promote breast cancer, ovarian cancer, endometrial cancer, etc. Tumor occurrence and developmentLipid metabolism is abnormally active in tumor tissue, which is one of the markers of malignant tumor metabolism, and high cholesterol intake is obviously related to the appearance of tumors. High cholesterol intake increases the risk of pancreatic and ovarian cancer. Cholesterol also plays a crucial role in tumor cell proliferation, invasion and drug resistance.
The content and composition of cholesterol in tumor tissues and cancer cells are different from those in normal tissues. The oxidation products of cholesterol can promote or inhibit glucocorticoid receptors and estrogen receptors by regulating glucocorticoid receptors and estrogen receptors. tumor progression. Compared with non-tumor cells, tumor cells can produce more cancer-promoting oxidized cholesterol and less tumor suppressor oxidized cholesterol. Dyslipidemia can provide more cholesterol to cancer cells, induce cancer cells to produce more pro-cancer oxidized cholesterol, thereby increasing the risk of tumorigenesis.
Tumor treatment can cause hyperlipidemia. Common factors include chemotherapy drugs, endocrine therapy drugs, targeted drugs, immunotherapy, and radiotherapy. Antitumor therapy causes dyslipidemia to increase cardiovascular events.
In the treatment of hormone receptor-positive postmenopausal breast cancer patients, the incidence of hyperlipidemia and the incidence of cardiovascular events were higher than those of normal women, including fatal myocardial infarction, Q-wave myocardial infarction, non-Q-wave myocardial infarction, unstable angina pectoris or severe angina pectoris requiring revascularization, essential hypertension, arrhythmia, etc. In the treatment of prostate patients, the levels of TG, TC, HDL-c, and low-density lipoprotein cholesterol (LDL-c) were higher than those of normal men, respectively.
Because there are currently no guidelines and norms for blood lipid control in cancer patients at home and abroad, it is recommended that the main control target of dyslipidemia in cancer patients be listed as LDL-c, the secondary target Listed as non-HDL-c. There is also no anti-tumor drug dyslipidemia risk stratification standard at home and abroad. Due to the high risk of dyslipidemia caused by drugs such as lorlatinib and L-asparaginase, special precautions should be taken when using them. Most of the anti-tumor drugs have little related clinical research evidence on dyslipidemia, and they are temporarily classified as low-risk dyslipidemia anti-tumor drugs. 02—Non-drug interventions for abnormal blood lipid levels in cancer patients are mainly lifestyle interventions, including smoking cessation, maintaining ideal body weight or weight loss, exercise , adjust the diet structure, etc.
Adjust the diet structure and maintain the ideal body weight: through low-carbohydrate high-quality protein diet and aerobic exercise Maintaining body weight, keeping the BMI between 20 kg/m2 and 24 kg/m2, increasing the intake of various fruits, vegetables, mushrooms and nuts, and adjusting the diet structure are conducive to reaching the blood lipid target. Aerobic exercise includes at least 150 minutes of moderate-intensity aerobic exercise per week, such as walking, jogging, cycling, swimming, dancing, etc.
If lifestyle adjustment fails to achieve blood lipid targets, lipid-lowering drug therapy should be initiated. Lipid-lowering drugs mainly include statins, fibrates, niacin, bile acid chelators, and intestinal cholesterol absorption inhibitors.
✔ For high-risk dyslipidemia drugs, the monitoring period is short; for low-risk dyslipidemia drugs, the monitoring period is short, the initial monitoring period is 4 to 6 weeks, and 4 to 6 weeks after administration of lipid-lowering drugs Weekly review of blood lipids, liver function, and creatine kinase, if there are no special circumstances, and blood lipid levels meet the standard, the monitoring period can be extended to review once every 3 to 6 months, and those who continuously meet the standard can be reviewed once a year.
✔ The initial monitoring period of anti-tumor drugs for low-risk dyslipidemia is 4 to 8 weeks, and blood lipids, liver function, creatine should be reviewed 4 to 8 weeks after administration of lipid-lowering drugs. For kinases, if there are no special circumstances and the blood lipid level reaches the standard, the monitoring period can be extended to review once every 6 to 12 months, and those who continuously meet the standard can be reviewed once a year. Paying attention to the control of abnormal blood lipid levels in cancer patients will help improve the prognosis of patients. Oncology clinicians need to strengthen the awareness of identifying dyslipidemia caused by common anti-tumor drugs, to ensure that patients’ blood lipid levels are well controlled during anti-tumor drug treatment, and to ensure the safety of anti-tumor drug treatment programs.
Li Suyi, MD
Department of Tumor Nutrition and Metabolic Therapy
The First Affiliated Hospital of China University of Science and Technology, West District