Case report
Hyperphosphatemia during spontaneous tumor lysis syndrome culminate in severe hypophosphatemia at the time of blast crisis of Phneg CML to acute myelomoncytic leukemia
1 The Amalia Biron Research Institute of Thrombosis and Hemostasis, Sheba Medical Center and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
2 Institute of Nephrology and Hypertension, Sheba Medical Center and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
3 Department of Pathology, Sheba Medical Center and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
4 Hematology Laboratory, Sheba Medical Center and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
5 Institute of Hematology, Sheba Medical Center and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
6 Department of Diagnostic Imaging, Sheba Medical Center and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
7 Department of Internal Medicine D, Sheba Medical Center and Sackler Faculty of Medicine Tel Aviv University, Tel Aviv, Israel
Experimental Hematology & Oncology 2012, 1:24 doi:10.1186/2162-3619-1-24
Published: 29 August 2012Abstract
Extreme swing of phosphor from severe hyperphosphatemia to severe hypophosphatemia in a patient with blast crisis of myeloid origin was the result of imbalance between massive apoptosis of leukemic cells in the context of spontaneous tumor lysis syndrome and massive production of leukemic cells with only 1% of blast in peripheral blood. The mutated p53 protein suggested acting as oncogene in the presented case and possibly affecting phosphor status.
