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Open Access Highly Accessed 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

Ophira Salomon1*, Eli J Holtzman2, Pazit Beckerman2, Camila Avivi3, Luba Trakhtenbrot4, Abraham Kneller5, Tali Tohami4, Yeroham Kleinbaum6, Sara Apter6, Ninette Amariglio4, Ehud Grossman7 and Ginette Schiby3

Author Affiliations

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

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Experimental Hematology & Oncology 2012, 1:24  doi:10.1186/2162-3619-1-24

Published: 29 August 2012

Abstract

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.

Keywords:
Acute leukemia; Tumor lysis syndrome; Apoptosis; Hypophosphatemia; Hyperphosphatemia