Pathophysiology, clinical consequences, and treatment of tumor lysis syndrome

Davidson, Michael; Thakkar, Snehal Govind; Hix, John K.; Bhandarkar, Naveen D.; Wong, Alina; Schreiber, Martin J.

doi:10.1016/j.amjmed.2003.09.045

Cited by 280 publications

(286 citation statements)

References 68 publications

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“…1 The standard management of hyperuricemia consists of hydration, alkalinization of the urine and the administration of allopurinol. Allopurinol, available in oral as well as intravenous formulations, affects purine metabolism by inhibiting xanthine oxidase, an enzyme responsible for the conversion of hypoxanthine to xanthine, and xanthine to uric acid.…”

Section: Introductionmentioning

confidence: 99%

Reduced-dose rasburicase (recombinant xanthine oxidase) in adult cancer patients with hyperuricemia

Trifilio

Singhal

et al. 2006

Bone Marrow Transplant

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Recombinant urate oxidase (rasburicase) lowers uric acid levels rapidly to very low levels at the labeled dose of 0.15-0.2 mg/kg daily for 5 days. Our past experience showed that a lower dose (3 mg) lowered uric acid levels sufficiently in most patients. A retrospective review was conducted to determine the effect of a fixed 3 mg dose of rasburicase in 43 adult patients with cancer undergoing hematopoietic stem cell transplantation or receiving chemotherapy who had elevated or rising uric acid levels (6.4-16.8 mg/dl; median 9.6). Six patients received a second dose of rasburicase (3 mg in four patients and 1.5 mg in two patients) 24 h later. Patients received allopurinol, adequate hydration, as well as other supportive therapy as required. Uric acid levels declined by 6-95% (median 43%) within the first 24 h after rasburicase administration, and levels at 48 h were 9-91% (median 65%) lower than the baseline levels. Serum creatinine changed by p10% in 21 patients, increased by 410% in four patients and decreased by 410% in 18 patients. No significant renal dysfunction developed in any of the patients. We conclude that rasburicase is effective in lowering uric acid levels at a fixed dose of 3 mg, which is much lower than the recommended dose.

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Section: Introductionmentioning

confidence: 99%

Reduced-dose rasburicase (recombinant xanthine oxidase) in adult cancer patients with hyperuricemia

Trifilio

Singhal

et al. 2006

Bone Marrow Transplant

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“…Increase of uric acid in acute leukemia may be due to the increase Tumor Lysis Syndrome (TLS), which is an oncologic emergency that is caused by massive tumor cell lysis with the release of large amounts of potassium, phosphate, and nucleic acids into the systemic circulation [15]. Catabolism of the nucleic acids to uric acid leads to hyperuricemia; the marked increase in uric acid excretion can result in the precipitation of uric acid in the renal tubules and renal vasoconstriction, impaired autoregulation decreased renal flow, oxidation, and inflammation, resulting in acute kidney injury [16].…”

Section: Discussionmentioning

confidence: 99%

Acute Renal and Hepatic Failure and Abnormal Blood Cell Count in Acute Leukemia: A Report of Four Cases and Review of the Literature

Elbossaty¹

2017

J Pharma Care Health Sys

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Leukemia is white blood cells cancer, which characterized with production of immature blood cells. Overcrowding of bone marrow with this abnormal immature cells, which interference with normal blood cells production, this may be lead to hyperleukocytosis, cytopenias, liver and kidney failure. In this study reports a case series of four patients with acute leukemia were studied. From this study, we concluded that hyperleukocytosis and cytopenias, disturbance in liver and kidney function were correlated with ALL than in AML.

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“…Both electrolyte abnormalities usually develop 24 to 48 h after chemotherapy. Hyperphosphatemia results from rapid release of intracellular phosphates into the peripheral blood during acute degradation of malignant cells, which may contain up to four times more organic and inorganic phosphates as compared to normal cells (Yarpuzlu, 2003;Davidson, 2004).…”

Section: Hyperphosphatemia and Hypocalcemiamentioning

confidence: 99%

Tumour Lysis Syndrome: Implications for Cancer Therapy

Mika¹,

Ahmad²,

Guruvayoorappan³

2012

Asian Pacific Journal of Cancer Prevention

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Asian Pacific J Cancer Prev, 13, 3555-3560 IntroductionTumour lysis syndrome (TLS) is the development of an array of metabolic disturbances that may occur either spontaneously or in response to cancer therapies. It results when a huge number of rapidly dividing cancer cells, particularly leukemia and lymphoma, are killed or lysed by cytotoxic therapy such as chemotherapy and radiation. Normal intracellular components of cells include potassium, phosphorus and nucleic acids. These intracellular ions are present in large amounts in cancer cells as compared to those in normal cells.When malignant cells are killed by therapy they release their contents into the systemic circulation, which accumulate faster in the body than being eliminated from the body and the body's homeostatic mechanisms find it difficult to cope with. The release of these intracellular contents cause metabolic disturbances, which in turn manifest into life threatening complications such as hyperkalemia, hyperphosphotemia, hypocalcemia and hyperuricemia. Tumour lysis also releases cytokines that cause a systemic inflammatory response syndrome and often multiorgan failure (Hijiya et al., 2005;Nakamura et al., 2009;Soares et al., 2009).During the early stages, some patients do not experience any symptoms of TLS but have abnormal laboratory values, which is suggestive of its succession. Laboratory results will show high potassium, uric acid and phosphorus levels and low calcium levels in the blood.

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Pathophysiology, clinical consequences, and treatment of tumor lysis syndrome

Cited by 280 publications

References 68 publications

Reduced-dose rasburicase (recombinant xanthine oxidase) in adult cancer patients with hyperuricemia

Reduced-dose rasburicase (recombinant xanthine oxidase) in adult cancer patients with hyperuricemia

Acute Renal and Hepatic Failure and Abnormal Blood Cell Count in Acute Leukemia: A Report of Four Cases and Review of the Literature

Tumour Lysis Syndrome: Implications for Cancer Therapy

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