Lipid profile changes in patients with acute leukemia after pathogenetic therapy

Aim. To study changes in lipid profile in patients with acute leukemia who received pathogenetic therapy.

Material and methods. The study included 13 patients diagnosed with acute leukemia who underwent pathogenetic therapy, including multiagent chemotherapy and allogeneic hematopoietic stem cell transplantation. The median age was 40 years. All patients in the study group underwent an assessment of lipid profile, as well as an assessment of liver and kidney function at the time of diagnosis, the end of chemotherapy courses, and after allogeneic hematopoietic stem cell transplantation.

Results. Total cholesterol, triglyceride, very low-density lipoprotein and lowdensity lipoprotein values in the study groups significantly change over time at different stages of treatment. Total cholesterol values have a higher risk of increasing in patients with acute leukemia at the end of chemotherapy and after allogeneic hematopoietic stem cell transplantation compared to the disease onset. Patients with acute leukemia significantly more often have an increase in total cholesterol and triglyceride levels by the end of chemotherapy and after allogeneic hematopoietic stem cell transplantation.

Discussion. Increased cardiovascular risk in patients with acute leukemia receiving pathogenetic therapy, including allogeneic hematopoietic stem cell transplantation, is associated with high antitumor therapy toxicity, and is also a consequence of the neoplastic process. Hypolipidemia at the onset of acute leukemia is primarily associated with their increased consumption by neoplastic cells. Impaired liver function and decreased glomerular filtration rate during treatment of acute leukemia are largely associated with highly toxic regimens of antitumor therapy.

Conclusion. In patients with acute leukemia at different stages of pathogenetic treatment, including polychemotherapy and allogeneic hematopoietic stem cell transplantation, the development of lipid metabolism disorders is the pathogenetic basis for the formation of cardiovascular complications.

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