Rasburicase-induced Hemolytic Anemia in an Adolescent With Unknown Glucose-6-Phosphate Dehydrogenase Deficiency

Akande, Manzilat; Audino, Anthony; Tobias, Joseph D.

doi:10.5863/1551-6776-22.6.471

Cited by 6 publications

(11 citation statements)

References 31 publications

(35 reference statements)

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“…The most efficient therapy for dramatically lowering uric acid is Rasburicase, a recombinant form of urate oxidase, a nonhuman proteolytic enzyme that oxidizes uric acid to allantoin, and a metabolite that is far more soluble than uric acid. Rasburicase is contraindicated in patients with G6PD deficiency (G6PDD) due to risk of drug induced hemolytic anemia [17]. G6PD level was however not checked before administering Rasburicase in our patient.…”

Section: Discussionmentioning

confidence: 97%

Acute Uric Acid Nephropathy following Epileptic Seizures: Case Report and Review

Patel

Wilson

Ahmed

et al. 2019

Case Reports in Nephrology

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Acute hyperuricemia most commonly occurs in patients who experience tumor lysis syndrome. Hyperuricemia along with other electrolyte abnormalities like hyperkalemia, hypocalcemia, and hyperphosphatemia leads to acute kidney injury (AKI) due to acute uric acid nephropathy which is associated with significant morbidity. High risk patients are thus closely monitored for signs of these laboratory abnormalities. Extreme exercise, rhabdomyolysis, and seizures are rare causes of acute hyperuricemia. Serum uric acid level is not routinely monitored as a part of postictal labs. We report an unusual case of AKI in a young male with recurrent seizures and no associated rhabdomyolysis who was found to have acute uric acid nephropathy. Timely administration of Rasburicase prevented the need for dialysis in this patient and led to complete renal recovery. This case illustrates the importance of doing a urine microscopy and checking uric acid level in patients with recurrent seizures who develop unexplainable AKI, as timely management helps improve outcome. We also briefly review the pathophysiology of seizure related hyperuricemia and acute uric acid nephropathy.

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Section: Discussionmentioning

confidence: 97%

Acute Uric Acid Nephropathy following Epileptic Seizures: Case Report and Review

Patel

Wilson

Ahmed

et al. 2019

Case Reports in Nephrology

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“…Methemoglobinemia is a rare complication of G6PD deficiency following use of rasburicase. In converting uric acid to allantoin, rasburicase produces hydrogen peroxide, which causes oxidative damage in G6PD-deficient red blood cells [ 24 ]. Methylene blue is typically the first-line treatment for methemoglobinemia, but it requires reduction to leucomethylene blue by NADPH.…”

Section: Discussionmentioning

confidence: 99%

Glucose-6-phosphate dehydrogenase deficiency presenting with rhabdomyolysis in a patient with coronavirus disease 2019 pneumonia: a case report

Chen

Evans

et al. 2022

J Med Case Reports

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Background Glucose-6-phosphate dehydrogenase deficiency is a rarely recognized predisposing factor for rhabdomyolysis. Rhabdomyolysis with coronavirus disease 2019 has been increasingly seen during the pandemic. We report the uncommon occurrence of coronavirus disease 2019 pneumonia, severe rhabdomyolysis, and acute renal failure in the setting of glucose-6-phosphate dehydrogenase deficiency. Case presentation A 19-year-old African American male presented with myalgias, diaphoresis, and dark urine. Testing for severe acute respiratory syndrome coronavirus 2 was positive. He had severe rhabdomyolysis with creatine kinase levels up to 346,695 U/L. He was oliguric and eventually required hemodialysis. Progressive hypoxemia, methemoglobinemia, and hemolytic anemia occurred following one dose of rasburicase for hyperuricemia. Glucose-6-phosphate dehydrogenase deficiency was diagnosed. Full recovery followed a single volume exchange transfusion and simple packed red blood cell transfusions. Conclusions Glucose-6-phosphate dehydrogenase deficiency may predispose individuals to rhabdomyolysis due to severe acute respiratory syndrome coronavirus 2, presumably due to altered host responses to viral oxidative stress. Early screening for glucose-6-phosphate dehydrogenase deficiency can be useful for management of patients with rhabdomyolysis.

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“…In G6PD‐deficient individuals, this can cause methemoglobinaemia and acute haemolysis, which can be fatal. Multiple case reports describe G6PD‐deficient individuals who developed methemoglobinaemia and acute haemolysis after rasburicase treatment 9–18 . Therefore, rasburicase is currently contraindicated in patients with G6PD deficiency and carries an FDA boxed warning 5,19…”

Section: Introductionmentioning

confidence: 99%

“…Multiple case reports describe G6PD-deficient individuals who developed methemoglobinaemia and acute haemolysis after rasburicase treatment. [9][10][11][12][13][14][15][16][17][18] Therefore, rasburicase is currently contraindicated in patients with G6PD deficiency and carries an FDA boxed warning. 5,19 The FDA recommends that patients of certain ancestries (e.g., African or Mediterranean) be tested for G6PD deficiency prior to rasburicase administration, 19 since these populations have a higher prevalence of this enzyme deficiency.…”

mentioning

confidence: 99%

Impact of pre‐emptive rapid testing for glucose‐6‐phosphate dehydrogenase deficiency prior to rasburicase administration at a tertiary care centre: A retrospective study

Ganapathi

Campbell

Ofori

et al. 2022

Brit J Clinical Pharma

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Aims Glucose‐6‐phosphate dehydrogenase (G6PD) deficiency, the most common enzymopathy in humans, can cause acute haemolysis resulting from exposure to certain medications, chemicals, infections and fava beans. Rasburicase, used to manage elevated uric acid levels in the oncologic emergency of tumour lysis syndrome, is one such drug. The US Food and Drug Administration (FDA) recommends testing of G6PD status prior to rasburicase administration for patients at higher risk for G6PD deficiency. Methods We performed a retrospective chart review of all oncology patients for whom a semi‐quantitative biochemical test for detecting G6PD deficiency was performed prior to rasburicase administration over a 2.5‐year period, in a large academic metropolitan hospital. Results We identified 16 out of 260 tested individuals as G6PD‐deficient (6.1%), including six females. On average, test results were electronically available to health care providers within 4 hours of sample collection, with most results available within 2–3 hours. Four G6PD‐deficient patients developed elevated uric acid levels. Two of the G6PD‐deficient patients were treated with rasburicase, and subsequently developed haemolysis, which was appropriately managed. Conclusion In summary, by providing information about G6PD status with a rapid turnaround time, we have taken a significant step towards personalized medicine in our institution. In spite of the test implementation, two out of four G6PD‐deficient patients, who were no longer candidates for rasburicase use, still received the drug, highlighting the need for improved provider education.

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Rasburicase-induced Hemolytic Anemia in an Adolescent With Unknown Glucose-6-Phosphate Dehydrogenase Deficiency

Cited by 6 publications

References 31 publications

Acute Uric Acid Nephropathy following Epileptic Seizures: Case Report and Review

Acute Uric Acid Nephropathy following Epileptic Seizures: Case Report and Review

Glucose-6-phosphate dehydrogenase deficiency presenting with rhabdomyolysis in a patient with coronavirus disease 2019 pneumonia: a case report

Impact of pre‐emptive rapid testing for glucose‐6‐phosphate dehydrogenase deficiency prior to rasburicase administration at a tertiary care centre: A retrospective study

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