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Blister and bite cells in G6PD deficiency

A 40yearold man presented with a newly diagnosed diffuse large Bcell lymphoma with involvement of the cervical lymph nodes. Serum chemistry analysis showed an elevated uric acid level (100 mg/L), and the patient was started on rasburicase for treatment of presumptive tumor lysis syndrome (TLS). One day after initiation of rasburicase, the patient developed symptomatic methemoglobinemia (increased methemoglobin to 8.4%, reference <1.0%) and hemolytic anemia [hemoglobin 75 g/L, increased lactate dehydrogenase 632 units/L, and decreased haptoglobin <50 mg/L (reference 1602000 mg/L)]. A peripheral blood smear demonstrated anemia with marked anisopoikilocytosis including numerous blister cells (irregularly contracted hemoglobin with regional clearing on one side) and occasional bite cells (keratocytes, Figure 1). Further investigation revealed glucose6phosphate dehydrogenase (G6PD) deficiency via qualitative assay of visual fluorescence of G6PD using the Trinity Biotech procedure (Category 203A). The characteristic findings of “blister” and “bite” cells represent oxidative damage to red blood cells induced by rasburicase (a recombinant form of urate oxidase) which converts uric acid into a watersoluble allantoin and produces hydrogen peroxide; the latter oxidizes the sulfhydryl group on hemoglobin, leading to methemoglobin formation1 and precipitated denatured hemoglobin forming Heinz bodies that are invisible on a routinely stained smear. Patients with G6PD deficiency are at risk for sustained methemoglobinaemia and oxidative hemolysis due to depletion of glutathione (a vital antioxidant) and impaired ability to reduce methemoglobin to hemoglobin.2 Baseline G6PD activity should be obtained in patients who are considered high risk for TLS prior to receiving rasburicase. Prevention and management of TLS require a multifaceted approach, including aggressive hydration and alternative use of allopurinol (a xanthine oxidase inhibitor).