Hyperphosphatemia during spontaneous tumor lysis syndrome culminate in severe hypophosphatemia at the time of blast crisis of Phneg CML to acute myelomoncytic leukemia

Severe symptomatic hypophsopahatemia was reported in a small number of case reports in patients with acute myelomonocytic leukemia [1] with extreme white blood count (200-380/μL) because of high phosphate demands of dividing leukemic cells. It was also reported during hematopoietic reconstitution after allogeneic peripheral blood stem cell transplantation [2] due to excessive cellular phosphate uptake for hematopoietic reconstitution and in tumor genesis [1].Leukemic blast cells of myeloid origin fail to show inhibition of glycolysis by oxygen [3] and causes hypophosphatemia by redistribution of phosphorus to the cells, to provide phosphate for glycolytic intermediates.Severe hypophosphatemia may adversely affect major organ systems including severe generalized muscle weakness as observed in our patient. Reduction in the erythrocyte content of 2,3-diphosphoglycerate may impair release of oxygen resulting in hypoxia [4]. On the other hand hyperleukocytosis can cause pseudohyposphatemia, pseudohypokalemia [5] and pseudohypoxaemia. Unawareness to this phenomenon can lead to incorrect and harmful treatment.An 80-year-old white Ashkenazi Jewish woman presented at hematology out-patient clinic with persistent leukocytosis for the last 10？months. A peripheral blood count revealed white-cell count (WBC) of 36,000/μL with 58% neutrophils, 14% lymphocytes, 4% monocytes, 1% blasts, 2% metamyelocytes, 6% myelocytes and 10% segments. The hemoglobin was 12gr/dL, platelet counts 476,000/μL and blood chemistry was unremarkable. Her physical examination was normal as well as whole body computerized tomography scanning (CT). Bone marrow (BM) aspiration at that time was hyperplastic, enriched with white cells with normal maturation and no blasts. Megakaryocytes had dysplastic features with single nucleous without lobulations. The BM findings were compatible with a myeloproliferative disorder with some dysplastic changes. Cytogenetic analysis revealed 47XX in 75% of the cells with tris