O'Regan S, Carson S, Chesney R W, Drummond K N
Blood. 1977 Mar;49(3):345-53.
Electrolyte disturbances in leukemia can be the result of the disease process or drug therapy. One group of electrolyte abnormalities is related to the stage of the leukemic process. Included in this group are newly diagnosed patients who may show elevated serum potassium, phosphorus, and magnesium--a result of their release from malignant cells after cytotoxic therapy or their accumulation due to urate nephropathy. Patients in remission usually have normal serum electrolyte concentrations, but acute leukemia patients during relapse may have hypokalemia, hypophosphatemia, and hypomagnesemia. This imbalance may be related to cellular uptake of these electrolytes in the presence of inadequate dietary intake. Other factors contributing to electrolyte derangements, and related to the leukemic process, include hyponatremia and hypochloremia secondary to the SIADH, hypokalemia in acute monocytic or acute myelomonocytic leukemia due to lysozyme-induced tubular damage, hypercalcemia possibly secondary to leukemic infiltration of bone or parathyroid glands (with PTH release), or production of a PTH-like substance by leukemic cells. Nonspecific factors related to the disease process which may aggravate the electrolyte imbalance include gastrointestinal loss through nausea, vomiting, and malnutrition. The drug-related electrolyte abnormalities include cyclophosphamide- and vincristine-induced SIADH; decreased serum sodium, chloride, potassium, and calcium concentrations as a result of polymyxin B nephrotoxicity; hypokalemia and hypomagnesemia secondary to amphotericin B; hypocalcemia, hypophosphatemia, and hyperphosphaturia due to L-asparaginase-induced hypoparathyroidism; hypokalemia due to a nonreabsorbable anion effect of antibiotics in the distal tubule or changes in membrane ionic transport of all cells by large doses of antibiotics. Electrolyte disturbance in leukemia thus have a multifactorial pathogenesis which can best be delineated according to the stage of the leukemic process and the drugs being used. Recognition of the cause or causes in a particular patient is essential for an effective approach to management. This review emphasizes the need for routine measurement of serum electrolytes during all phases of the leukemic process.
白血病中的电解质紊乱可能是疾病进程或药物治疗的结果。一组电解质异常与白血病进程的阶段有关。这组包括新诊断的患者，他们可能表现出血清钾、磷和镁升高，这是细胞毒性治疗后恶性细胞释放或尿酸肾病导致其蓄积的结果。缓解期患者的血清电解质浓度通常正常，但急性白血病复发期患者可能出现低钾血症、低磷血症和低镁血症。这种失衡可能与这些电解质在饮食摄入不足情况下的细胞摄取有关。其他导致电解质紊乱且与白血病进程相关的因素包括抗利尿激素分泌异常综合征继发的低钠血症和低氯血症、急性单核细胞白血病或急性粒单核细胞白血病因溶菌酶诱导的肾小管损伤导致的低钾血症、可能继发于白血病浸润骨骼或甲状旁腺（伴有甲状旁腺激素释放）的高钙血症，或白血病细胞产生的类甲状旁腺激素物质。与疾病进程相关的非特异性因素可能会加重电解质失衡，包括因恶心、呕吐和营养不良导致的胃肠道丢失。与药物相关的电解质异常包括环磷酰胺和长春新碱诱导的抗利尿激素分泌异常综合征；多粘菌素B肾毒性导致血清钠、氯、钾和钙浓度降低；两性霉素B继发的低钾血症和低镁血症；L-天冬酰胺酶诱导的甲状旁腺功能减退导致的低钙血症、低磷血症和高磷尿症；抗生素在远端小管的不可吸收阴离子效应导致的低钾血症或大剂量抗生素引起的所有细胞的膜离子转运变化。因此，白血病中的电解质紊乱具有多因素发病机制，最好根据白血病进程的阶段和所使用的药物来描述。识别特定患者的病因对于有效的治疗方法至关重要。本综述强调在白血病进程的所有阶段都需要常规测量血清电解质。
