Carta Acesso aberto Revisado por pares

Tumor lysis syndrome: current perspective

2007; Ferrata Storti Foundation; Volume: 93; Issue: 1 Linguagem: Inglês

10.3324/haematol.12327

ISSN

1592-8721

Autores

Jessica Hochberg, Mitchell S. Cairo,

Tópico(s)

Neutropenia and Cancer Infections

Resumo

T umor lysis syndrome is characterized by a group of metabolic derangements caused by the massive and abrupt release of cellular components into the blood following the rapid lysis of malignant cells.It is observed most frequently in patients with hematologic malignancies such as acute lymphoblastic leukemia (ALL) and Burkitt's lymphoma after the initiation of chemotherapy, although it may also occur in other malignancies, both hematologic and solid tumors.2][3][4][5] In some cases, tumor lysis syndrome can lead to acute renal failure and even death.The key to the management of tumor lysis syndrome includes awareness of its causes, identification of high-risk patients, implementation of appropriate prophylactic measures, vigilant monitoring of electrolyte levels in patients undergoing chemotherapy, and initiation of more active treatment measures when necessary. Pathophysiology7][8][9] The increased concentrations of uric acid, calcium, phosphates, potassium, and urea can overwhelm the body's homeostatic mechanisms to process and excrete these materials and result in the clinical spectrum associated with tumor lysis syndrome. 10Hyperuricemia and its associated complications are the most frequently recognized manifestations of tumor lysis syndrome, and predispose to many of the other clinical derangements.Hyperuricemia results from rapid release and catabolism of intracellular nucleic acids.][13][14] Hyperphosphatemia results from the rapid release of intracellular phosphates from malignant cells, which may contain as much as four times the amount of organic and inorganic phosphates as normal cells. 9,15Hyperphosphatemia can lead to the development of acute renal failure after precipitation with calcium in renal tubules during tumor lysis syndrome.The serum concentration of calcium rapidly decreases as precipitation with phosphate occurs.Hypocalcemia is one of the most serious clinical manifestations of tumor lysis syndrome and has been associated with the development of severe muscle cramping, tetany, and cardiac arrhythmias.Hyperkalemia may also be a life-threatening consequence of tumor lysis syndrome.Hyperkalemia results from the kidneys' inability to clear the massive load of intracellular potassium released by lysed tumor cells.Neuromuscular signs and symptoms may include muscle weakness, cramps, paresthesias, and possible paralysis.Cardiac manifestations may include asystole, ventricular tachycardia or fibrillation, syncope, and possible sudden death. 5,15ncreases in blood urea nitrogen and creatinine levels occur as a result of renal impairment associated with acute uric acid crystal nephropathy, calcium-phosphate crystals and nephrocalcinosis, or a combination of both, leading to an acute obstructive uropathy syndrome.Acute clinical manifestations may include uremia, edema, hypertension, congestive heart failure, and exacerbations of metabolic disturbances. DefinitionWhile the set of metabolic abnormalities comprising tumor lysis syndrome is generally agreed upon, there is currently no universally accepted system for classifica-

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