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HERO ID
2056537
Reference Type
Journal Article
Subtype
Review
Title
The management of tumor lysis syndrome
Author(s)
Rampello, E; Fricia, T; Malaguarnera, M
Year
2006
Is Peer Reviewed?
1
Journal
Nature Clinical Practice Oncology
ISSN:
1743-4254
EISSN:
1743-4262
Volume
3
Issue
8
Page Numbers
438-447
Language
English
PMID
16894389
DOI
10.1038/ncponc0581
Web of Science Id
WOS:000239341100010
Abstract
The manifestation of tumor lysis syndrome (TLS) occurs when the destruction of tumor cells releases breakdown products that overwhelm the excretory mechanisms of the body. A cardinal sign is hyperuricemia, leading to uric acid nephropathy. Other signs are hyperkalemia, hyperphosphatemia and secondary hypocalcemia. Conventional management of TLS consists of aggressive intravenous hydration, diuretic therapy, urinary alkalization, and inhibition of urate production by high-dose allopurinol. Urate oxidase has been used in the management of patients at risk for TLS and recently the recombinant urate oxidase rasburicase was developed. Several data indicate that rasburicase is effective and well tolerated in the prevention and treatment of chemotherapy-induced hyperuricemia. Treatment options of hyperkalemia include sodium polystyrene sulfonate, hypertonic glucose and insulin, loop diuretics, and bicarbonate. Treatment of hyperphosphatemia reduces dietary phosphate intake and includes phosphate binders such as aluminum hydroxide and aluminum carbonate. When recurrent hypocalcemia is present, a continuous intravenous infusion of calcium gluconate can be initiated. Hemodialysis should be considered for every patient with excessively elevated uric acid, phosphate and/or potassium and in those patients with acute renal failure to control urinary volume and manage uremia.
Keywords
acute renal failure; hyperkalemia; hyperuricemia; hypocalcemia; tumor lysis syndrome
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