Tumor Lysis

Tumor lysis syndrome is usually seen 1-5 days after the initiation of chemotherapy in patients with AML and high circulating blast counts.25 In response to chemotherapy, leukemic cells lyse, leading to hyper-phosphatemia, hyperkalemia (or hypokalemia), hypo-calcemia, an elevated lactate dehydrogenase (LDH), and hyperuricemia. Hyperuricemia results from breakdown of nucleotide precursors in leukemic cells to hypoxanthine and xanthine, and subsequent conversion to uric acid.25 Renal failure can occur secondary to precipitation of calcium phosphate crystals or uric acid in the renal tubules.25-28 Patients at risk for tumor lysis should be aggressively hydrated and started on allop-urinol. Allopurinol, an inhibitor of xanthine oxidase, decreases the production of uric acid.25 Rasburicase, a novel recombinant form of urate oxidase, converts uric acid to allantoin.25 Allantoin is five to ten times more soluble than uric acid, thus allowing for more rapid urinary excretion.25 29 Rasburicase should be considered for patients with renal dysfunction or high serum uric acid (i.e., >10).25 The drug should not be administered to patients with G6PD deficiency, as an additional by-product of the drug is hydrogen peroxide, which can lead to hemolytic anemia or methemoglobinemia in these patients.25 Alkalinizing the urine may also increase the solubility of uric acid.25 30 Electrolytes, uric acid, and LDH should be monitored carefully in tumor lysis syndrome.25 Any electrolyte abnormalities should be corrected appropriately.

activation of platelet-derived growth factor.4 46 This activation may lead to the megakaryocytic proliferation and fibrosis seen in acute megakaryocytic leukemia.446 These infants present with extensive organomegaly.4 Acute megakaryocytic leukemia is also the most common acute leukemia seen in patients with Down syndrome4748 and may be transient, resolving spontaneously.

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