Tumor Lysis Syndrome: New Challenges and Recent Advances

Abstract

Tumor lysis syndrome (TLS) is an oncologic emergency triggered by the rapid release of intracellular material from lysing malignant cells. Most common in rapidly growing hematologic malignancies, TLS has been reported in virtually every cancer type. Central to its pathogenesis is the rapid accumulation of uric acid derived from the breakdown of nucleic acids, which leads to kidney failure by various mechanisms. Kidney failure then limits the clearance of potassium, phosphorus, and uric acid leading to hyperkalemia, hyperphosphatemia, and secondary hypocalcemia, which can be fatal. Prevention of TLS may be more effective than treatment, and identification of at-risk individuals in whom to target preventative efforts remains a key research area. Herein, we discuss the pathophysiology, epidemiology, and treatment of TLS with an emphasis on the kidney manifestations of the disease.

Tumor Lysis Syndrome Following a Single Atezolizumab Infusion for Metastatic Urothelial Carcinoma Involving Both Upper and Lower Tract

“…Tumor lysis syndrome (TLS) is a potential complication in cancer therapy, which is caused by the sudden, rapid death of cells, occurs much more commonly in patients with aggressive non-Hodgkin's lymphomas, such as Burkitt's lymphoma, and leukemias, in response to cancer therapies [1][2][3][4][5][6][7][8][9]. TLS is characterized by hyperphosphatemia, hyperuricemia, hyperkalemia, hypocalcemia, lactic acidosis, acute renal failure (ARF) and increased mortality.…”

Concurrent acute spontaneous tumor lysis syndrome complicated with multiple organ failure in a patient with pre-existing undiagnosed lung cancer

“…Secondary hypocalcemia of TLS is the more immediate threatening of the two electrolytes disorders, leading in severe cases to arrhythmia, seizures, tetany and death. The hypocalcemia of TLS may persist even after phosphate levels normalize, presumably because of deficiencies of 1, 25-dihydroxyvitamin D [9]. In our patient, symptomatic hypocalcemia as focal motor seizures improved with 10 ml of intravenous 10 % calcium gluconate (containing 0.465 mEq/ml elemental calcium) and then inserted on oral calcium carbonate.…”

Radiation-Induced Tumor Lysis Syndrome in Chronic Lymphocytic Leukemia

“…TLS is diagnosed by both laboratory and clinical findings. Laboratory TLS is defined as the imbalance of two or more electrolytes (hypocalcemia, hyperuricemia, hyperphosphatemia, hyperkalemia), whereas clinical TLS is defined as laboratory TLS plus one clinical finding (increased creatinine, arrhythmia/sudden death, seizure) [4,5,6,7]. …”