BACKGROUND AND AIM: A wide array of disturbances in electrolyte equilibrium is commonly seen in patients with acute leukemia (AL). These abnormalities present a potential hazard in these patients, as that of enhancing the cardiotoxic effects of certain chemotherapeutic regimens. The literature dealing with AL-related electrolyte abnormalities and their interactions in leukemic patients was reviewed. DATA SYNTHESIS: Sources included MEDLINE and EMBASE. The search strategy was based on the combination of 'acute leukemia', 'electrolyte abnormalities', 'acid-base disorders', 'potassium', 'sodium', 'magnesium', 'calcium', and 'phosphorus'. References of retrieved articles were also screened. A decrease in serum potassium, mainly owing to lysozyme-induced tubular damage, appears to be one of the most frequent and potentially hazardous abnormalities. Other clinically significant metabolic perturbations include hyponatremia and hypercalcemia. CONCLUSION: A broad spectrum of electrolyte abnormalities is encountered in the clinical setting of AL, which are related to the disease process per se and/or to the therapeutic interventions. Clinicians should be vigilant for early detection and appropriate management of these disorders before the initiation of chemotherapy regimens as well as during treatment.
BACKGROUND AND AIM: A wide array of disturbances in electrolyte equilibrium is commonly seen in patients with acute leukemia (AL). These abnormalities present a potential hazard in these patients, as that of enhancing the cardiotoxic effects of certain chemotherapeutic regimens. The literature dealing with AL-related electrolyte abnormalities and their interactions in leukemicpatients was reviewed. DATA SYNTHESIS: Sources included MEDLINE and EMBASE. The search strategy was based on the combination of 'acute leukemia', 'electrolyte abnormalities', 'acid-base disorders', 'potassium', 'sodium', 'magnesium', 'calcium', and 'phosphorus'. References of retrieved articles were also screened. A decrease in serum potassium, mainly owing to lysozyme-induced tubular damage, appears to be one of the most frequent and potentially hazardous abnormalities. Other clinically significant metabolic perturbations include hyponatremia and hypercalcemia. CONCLUSION: A broad spectrum of electrolyte abnormalities is encountered in the clinical setting of AL, which are related to the disease process per se and/or to the therapeutic interventions. Clinicians should be vigilant for early detection and appropriate management of these disorders before the initiation of chemotherapy regimens as well as during treatment.