Background: Haematological malignancy affects lipid homeostasis representing elevated risks of cardiometabolic diseases. This study investigated the alteration of plasma lipids/lipoproteins and the underlying regulation mechanism. Materials and Methods: Blood samples were collected from acute myeloid leukaemia (AML) patients pre-and post-chemotherapy and matched controls. Triglyceride (TG), total cholesterol (TC), high-density-lipoprotein cholesterol (HDL-c), low-density-lipoprotein cholesterol (LDL-c) and apolipoproteins (apo) were quantified in plasma and lipoprotein-density-gradient fractions. The cardiometabolic risks and lipid loads were assessed. Results: Dyslipidaemia was revealed in 75% of AML patients pre-therapy by reduction of HDL-c and in 85% post-therapy by diverse combined patterns. Compared to the controls, AML patients exhibited increased plasma TG and cardiometabolic risks both pre- and post-therapy. The plasma TC, HDL-c, apoAI, B-100, CIII and J were decreased pre-therapy but were restored post-therapy. The plasma TG concentration was positively correlated with LDL-TG load, whereas plasma TC was positively correlated with HDL-c. Furthermore, the fractionated very-low-density lipoprotein (VLDL)-TG load was lower but LDL-TG load was higher in AML patients than in the controls, suggesting that circulating TG hydrolysis might be impaired from VLDL conversion to LDL. Conclusion: The plasma lipid profiles in AML were aberrant and predicted high cardiometabolic risks, which might need further follow-up attentions.