Plasma Lipid Profiling Increased Cardiometabolic Risks in Acute Myeloid Leukaemia Patients Pre- and Pro-chemotherapy

血液脂質分析顯示急性骨髓性白血病人，接受治療後增加心臟代謝疾病風險

血液惡性腫瘤影響脂質代謝平衡，導致心臟代謝疾病的風險升高。本研究目的為分析白血病患者治療過程血漿中脂質/脂蛋白的變化，及其潛在的調節機制與疾病的相關性。檢體來源為急性骨髓性白血病（AML）患者化療前後與健康對照組的血液樣本。本研究利用超高速密度梯度離心法分離脂蛋白，通過分析血漿三酸甘油脂（TG）、總膽固醇（TC）、高密度脂蛋白膽固醇（HDL-c）、低密度脂蛋白膽固醇（LDL-c）和載脂蛋白（apo），進行心臟代謝疾病風險評估和脂質恆定測試。分析結果顯示，在治療前，75%的AML患者呈現血脂異常，主要為HDL-c降低；而治療後，則有85% AML患者血脂異常並出現多樣組合模式。與健康對照組相比較，AML患者在治療前和治療後，TG與心血管代謝疾病的風險皆有升高的表現。同時，總膽固醇、高密度脂蛋白膽固醇、載脂蛋白apoAI、載脂蛋白B-100、載脂蛋白CIII和載脂蛋白J在治療前顯著降低，治療後與健康對照組則是沒有顯著差異。相關性分析結果顯示，血漿TG濃度與低密度脂蛋白TG含量，而血漿TC濃度與HDL-c出現正相關。此外，與健康對照組相比，AML患者的極低密度脂蛋白（VLDL）-TG負荷較低，但LDL-TG負荷較高，暗示在VLDL轉化為LDL的過程中TG水解可能受損。本研究結果顯示急性骨髓性白血病患者血液脂質代謝發生異常，可能增加併發心臟代謝疾病的風險，因此需要長期追蹤治療後病人的後續發展。

Background: Haematological malignancy affects lip id homeostasis representing elevated risks of cardiometabolic diseases. This study investigated the alteration of plasma lipids/lipoproteins and the underlying regulation mec hanism. Materials and Methods: B lood samples were collected fr om acute myeloid leukaemia(AML)patients pre- and post-chemotherapy and matched controls. Trigly ceride(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 f ractions. The cardiometabolic risks and lipid loads were assessed. Results: Dyslipidaemia was revealed in 75% of AML p atients pre-therapy by reduction of HDL-c and in 85% post-therapy by div erse combined patterns. Com pared 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 re stored post-therapy. The plasma TG concentration was positively correlated with LDL-TG load, whereas plasma TC was positively correlated with HDL-c. Furthermore, the fractio nated very-low-density lipoprot ein(VLDL)-TG load was lower but LDL-TG load was higher in AML pat ients than in the controls, sug gesting that circulating TG hydrolysis might be impaired from VLDL conv ersion to LDL. Conclusion: The plasma lipid profiles in AML were a berrant and predicted high cardiometabolic risks, which might need further follow-up attentions.