Tumor lysis syndrome.
Tumor lysis syndrome (TLS) is a constellation of metabolic disturbances observed in tumors with high cell turnover. It is associated with significant morbidity and mortality. TLS is characterized by the increased release of intracellular contents (uric acid, potassium, phosphorus) into the extracellular compartment, which can overwhelm the body's capacity for clearance. TLS is usually caused by response to chemotherapy; however, it may also occur spontaneously. Because uric acid, potassium, and phosphorus are excreted primarily by the kidneys, TLS can lead to hyperuricemia, hyperkalemia, and hyperphosphatemia with accompanying renal compromise. The pathophysiology of TLS-associated acute renal failure is probably multifactorial. Potential etiologies include intravascular volume depletion, urinary precipitation of nucleic acid metabolites and calcium phosphate, and malignancy-associated nephrotoxins. Despite prophylactic therapy with allopurinol and volume repletion, patients may still develop TLS with acute renal failure. While reducing the risk of uric acid precipitation, allopurinol and alkalinization increase the risk of xanthine and calcium phosphate crystals, respectively. Aggressive hydration might lead to volume overload, specifically in older patients. Novel approaches in the management of TLS include the use of urate oxidase, which can provide effective treatment with an acceptable safety profile.
Jeha
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Department of Pediatrics, University of Texas, M.D. Anderson Cancer Center, Houston, TX 77030, USA.
D000493:Allopurinol / Q000008:administration & dosage / Q000493:pharmacokinetics / Q000592:standards; D019337:Hematologic Neoplasms / Q000097:blood / Q000150:complications / Q000188:drug therapy; D006801:Humans; D012307:Risk Factors; D015275:Tumor Lysis Syndrome / Q000150:complications / Q000209:etiology* / Q000628:therapy*; D014503:Urate Oxidase / Q000008:administration & dosage / Q000592:standards
D000493:Allopurinol; D014503:Urate Oxidase