Hemolysis and Methemoglobinemia Secondary to Rasburicase Administration

Browning, Linda A; Kruse, James A.

doi:10.1345/aph.1g272

Cited by 82 publications

(67 citation statements)

References 11 publications

(13 reference statements)

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“…In the three cases where G6PD deficiency was known, hemolysis also developed. In those three cases, as with our patient, the hemolysis did not appear until after the methemoglobinemia (over 30 hr after rasburicase administration) [10][11][12]. Rasburicase has a t 1/2 of 18-24 hr and thus hydrogen peroxide may be generated for several days [8].…”

Section: Commentarysupporting

confidence: 67%

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Methemoglobinemia and hemolysis in a patient with G6PD deficiency treated with rasburicase

et al. 2012

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A 52-year-old African American male was admitted to the hospital for high-dose chemotherapy for refractory aggressive multiple myeloma (MM). He had previously progressed through bortezomib/dexamethasone and lenalidomide therapy. The most recent bone marrow biopsy showed approximately 90% kappa light chain-restricted plasma cells with a high proliferative rate (3.3% cells in S-phase). Admission labs prior to starting any therapy (Table I) were significant for uric acid 16.1 mg/ dL (reference range, 3.7-8.0), creatinine 2.1 mg/dL (reference range, 0.8-1.3 and his baseline was 1.1), lactate dehydrogenase (LDH) 438 U/L (reference range, 122-222), phosphorus 6.2 mg/dL (reference range, 2.5-4.5), hemoglobin 7.1 g/dL (reference range, 13.5-17.5), and IgG kappa monoclonal protein of 4.1 g/dL. On admission, baseline pulse oximetry at the bedside was normal at 95% O 2 saturation (SpO2). Due to baseline renal insufficiency and anticipated tumor lysis, intravenous (IV) fluids were started immediately followed by 6 mg of rasburicase on Day 1. High-dose IV cyclophosphamide (1,500 mg/m 2 ) and 1,000 mg of methylprednisolone were administered in the early morning on Day 2.This patient presents with hyperuricemia and hyperphosphatemia with laboratory levels that meet Cairo-Bishop criteria of tumor lysis syndrome (TLS) even before chemotherapy was initiated [1,2]. In addition, he also has an acute kidney injury (AKI) secondary to TLS occurring in the setting of refractory MM as manifested by high tumor burden, high plasma cell proliferative rate, increased serum LDH, and a very high uric acid with AKI.Given the clinical features and baseline hyperuricemia and AKI, rasburicase should be administered to prevent worsening renal failure. A glucose-6-phosphatase dehydrogenase (G6PD) level is usually obtained in patients receiving rasburicase because rasburicase can induce hemolysis and cause methemoglobinemia in enzyme-deficient individuals. In our patient, the options were to give rasburicase or to provide prophylactic kidney dialysis without rasburicase. We proceeded with rasburicase given the need for immediate chemotherapy.On hospital Day 2, bedside pulse oximetry showed significant hypoxemia (SpO2 75%), triggering an emergency consultation with the critical care team. The patient was evaluated and found to be quite comfortable on room air with a respiratory rate of 16 per minute without the use of accessory muscles of respiration; lung, cardiac, and mucous membrane examinations were normal. An arterial blood gas (ABG) was performed and the arterial blood was noted to be brown in color. ABG showed pH 7.39, pO 2 104 mmHg, pCO 2 39 mmHg, HCO 3 24 mmol/L and methemoglobin 12.9% (normal range, 0-1.5%). At this point, the care team discussed the use of IV methylene blue.

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Section: Commentarysupporting

confidence: 67%

“…Five of six patients required support with blood products. Methylene blue was given in two cases, one in a patient with known G6PD deficiency [9][10][11][12][13]. In the three cases where G6PD deficiency was known, hemolysis also developed.…”

Section: Commentarymentioning

confidence: 99%

Methemoglobinemia and hemolysis in a patient with G6PD deficiency treated with rasburicase

et al. 2012

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“…The former is readily excreted by the kidneys. The liberation of hydrogen peroxide can be devastating in patients with glucose-6-phosphate dehydrogenase deficiency, in whom the unchecked oxidative potential of H 2 O 2 can lead to methemoglobinemia and hemolytic anemia (60). Rasburicase will continue to be active in blood samples ex vivo, and thus inappropriately handled laboratory specimens may manifest spuriously low uric acid levels.…”

Section: Recombinant Urate Oxidasementioning

confidence: 99%

Onco-Nephrology

Wilson

Berns

2012

Clinical Journal of the American Society of Nephrology

121

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SummaryTumor lysis syndrome (TLS) describes the clinical and laboratory sequelae that result from the rapid release of intracellular contents of dying cancer cells. It is characterized by the release of potassium, phosphorous, and nucleic acids from cancer cells into the blood stream, with the potential to cause hyperkalemia; hyperphosphatemia and secondary hypocalcemia; hyperuricemia; AKI; and, should usual homeostatic mechanisms fail, death. TLS most commonly follows treatment of hematologic malignancies, such as acute lymphocytic or lymphoblastic leukemia, acute myeloid leukemia, and Burkitt lymphoma, but also occurs after treatment of other bulky or rapidly growing tumors, particularly if the patient is highly sensitive to the effects of cytotoxic chemotherapy. Prevention and treatment depend on prompt recognition of patients at risk, volume repletion, allopurinol, rasburicase (a novel recombinant urate oxidase), and, when indicated, dialysis.

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“…The most recently published data concerned with severe adverse reactions shows such responses to occur in less than 1 % of the population evaluated [ 824 ] . The most severe reactions to this drug are anaphylaxis, skin rashes, hemolysis, and methemoglobinemia [ 825,826 ] . Published data show skin rashes occur in about 1.4 % of patients undergoing treatment, bronchospasm occurs in less than 1 % of patients, and anaphylactic shock also occurs in less than 1 % of patients.…”

Section: Refractory Goutmentioning

confidence: 99%