Tumor Lysis Syndrome
Epidemiology
Tumor lysis syndrome usually occurs during chemotherapy or within 1-5 days after chemotherapy
Rare cases have been reported where tumor lysis occurs in the setting of spontaneous necrosis of a malignancy (without chemotherapeutic treatment)
Tumor lysis syndromes has been reported to occur with multiple agents
Fludarabine
Gemtuzumab
Glucocorticoids
Letrozole
Rituximab
Tamoxifen
Etiology
Treatment of Burkitt’s Lymphoma/Other Rapidly Proliferating Lymphomas (see Lymphoma )
Predictors of Tumor Lysis
Elevated Serum LDH (which is also correlated with tumor burden): >1500 IU/L
Hyperuricemia (which is also correlated with tumor burden)
Poor Renal Function
High Tumor Burden
Treatment of Acute Lymphocytic Leukemia (ALL) (see Acute Lymphocytic Leukemia )
Treatment of Acute Myeloid Leukemia (AML) (see Acute Myeloid Leukemia )
Treatment of Chronic Lymphocytic Leukemia (see Chronic Lymphocytic Leukemia )
Has been reported with Fludarabine treatment (see Fludarabine )
Treatment of Chronic Myeloid Leukemia (see Chronic Myeloid Leukemia ): occurs less commonly
Treatment of Solid Tumors: occurs less commonly
Physiology
Destruction of Large Number/Mass of Rapidly Proliferating Neoplastic Cells : increased turnover of nucleic acids -> hyperuricemia
Uric acid precipitation in renal tubules/medulla/collecting ducts (due to acidic local environment): may be exacerbated by dehydration and lactic acidosis
Clinical
Elevated Serum LDH
Levels >1500 IU/L -> predict development of tumor lysis syndrome in Burkitt’s lymphoma
Hyperuricemia (see Hyperuricemia )
Mechanism: increased turnover of nucleic acids from lysed cells
Hyperkalemia (see Hyperkalemia )
Mechanism: release of intracellular potassium
Hypocalcemia (see Hypocalcemia )
Mechanism: release of intracellular phosphate strores -> results in a reciprocal depression of serum calcium
Hyperphosphatemia (see Hyperphosphatemia )
Mechanism: release of intracellular phosphate strores -> results in a reciprocal depression of serum calcium
Lactic Metabolic Acidosis (see Metabolic Acidosis-Elevated Anion Gap and Lactic Acidosis )
Acute Kidney Injury (AKI) (see Acute Kidney Injury )
Mechanisms
Calcium Phosphate Deposition in Kidney
Hyperphosphatemia
Hyperuricemia with Uric Acid Crystal Deposition in Kidney
Diagnosis
Urinalysis: uric acid crystals is strong evidence for the presence of urate nephropathy
Urinary Uric Acid:Urinary Creatinine Ratio: >1 -> suggests urate nephropathy (while ratio <1 suggests AKI due to other causes)
Prognosis: excellent (once uric acid is decreased to <10 mg/dL)
Treatment
Monitoring
Follow serum chemistry q4-6hrs
Allopurinol (see Allopurinol )
May be used IV, in cases where PO therapy is not tolerated
IVF Hydration
Urine Alkalinization
Use D5W + 3 amps sodium bicarb per liter -> run at 250 ml/hr
Aim to maintain urine pH >7.0
May inadvertently promote urinary precipitation of calcium phosphate (which is less soluble at alkaline pH)
Rasburicase (Elitek) (see Rasburicase ): recombinant urate oxidase -> catalyzes conversion of uric acid to allantoin (which is soluble)
Decreases uric acid within hours
Dose: 0.2 mg/kg/day
Indications: tumor lysis syndrome where uric acid cannot be lowered by above therapies
Contraindications: G6PD deficiency (as these patients will be unable to break down the hydrogen peroxide end product of the urate oxidase reaction
Adverse Effects: bronchospasm, hypoxemia, hypotension
Hemodialysis : may be required in some cases
References
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