Report of two cases of rasburicase-induced methemoglobinemia

Kizer, Nora T.; Martinez, Emily; Powell, Matthew R.

doi:10.1080/10428190600967204

Cited by 31 publications

(26 citation statements)

References 7 publications

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“…RIM has been reported, as in our case, with doses as low as 6 mg, and although it can develop as early as 90 min after administration [9], several cases showed clinical manifestations more than 6 h following dosage [8,11]. This has implications for patients treated in the ambulatory care setting, in that 6 h of observation may not exclude the subsequent development of RIM after discharge.…”

Section: Discussionmentioning

confidence: 81%

“…Two patients were not tested, as G6PD deficiency was assumed: one due to the occurrence of the complication and African American ethnicity; the other case (ethnicity not specified) received concomitant primaquine and dapsone. Other enzymopathies were suggested (but not confirmed) as putative explanations for the manifestation of methemoglobinemia under oxidative stress [11]. All reported cases have recovered with resolution of methemoglobinemia, within 3-7 days, following cessation of rasburicase and supportive care.…”

Section: Discussionmentioning

confidence: 99%

“…G6PD deficiency is the most common disease causing enzymopathy in humans, affecting 400 million people worldwide, with Africa, South East Asia and the Mediterranean being the areas of highest prevalence [6]. Despite this prevalence, and the recent increased utilization of rasburicase, only 10 cases of methemoglobinemia have been reported to date, the majority of these in pediatric settings and few described in detail [4,7,8,9,10,11,12,13,14]. We report on a case of rasburicase-induced methemoglobinemia (RIM) and hemolytic anemia in an adult patient with (previously undiagnosed) G6PD deficiency.…”

Section: Introductionmentioning

confidence: 99%

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Rasburicase Causing Severe Oxidative Hemolysis and Methemoglobinemia in a Patient with Previously Unrecognized Glucose-6-Phosphate Dehydrogenase Deficiency

et al. 2013

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Rasburicase is frequently used in tumor lysis syndrome (TLS). Although it is very well tolerated, it can cause severe oxidative hemolytic anemia and methemoglobinemia in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency. We report another case of rasburicase-induced methemoglobinemia in a patient with previously unrecognized G6PD deficiency and review the cases of methemoglobinemia and oxidative hemolysis reported in the literature to date. Patients from ethnicities in which G6PD deficiency is prevalent at high risk of TLS should be screened for G6PD deficiency prior to administration of rasburicase where practical. Asymptomatic decrease in oxygen saturation by oximetry and cyanosis are signs of methemoglobinemia; patients recover with conservative measures including supplemental oxygen and packed red cell transfusion.

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Section: Discussionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Rasburicase Causing Severe Oxidative Hemolysis and Methemoglobinemia in a Patient with Previously Unrecognized Glucose-6-Phosphate Dehydrogenase Deficiency

et al. 2013

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“…It was first reported in patients with G6PD deficiency 2, but has also been seen in patients without G6PD deficiency 5, 8. The majority of cases are mild and treatment consists of supportive treatment with oxygen and red blood cell transfusions.…”

Section: Commentarymentioning

confidence: 99%

Rasburicase‐induced methemoglobinemia: case report, literature review, and proposed treatment algorithm

Sherwood

Paschal

Adamski

2016

Clinical Case Reports

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“…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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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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Report of two cases of rasburicase-induced methemoglobinemia

Cited by 31 publications

References 7 publications

Rasburicase Causing Severe Oxidative Hemolysis and Methemoglobinemia in a Patient with Previously Unrecognized Glucose-6-Phosphate Dehydrogenase Deficiency

Rasburicase Causing Severe Oxidative Hemolysis and Methemoglobinemia in a Patient with Previously Unrecognized Glucose-6-Phosphate Dehydrogenase Deficiency

Rasburicase‐induced methemoglobinemia: case report, literature review, and proposed treatment algorithm

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

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