PubMed · 1433712
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L J Rosenwasser, B Z Joseph. 1992-11-25. Immunohematologic diseases.. https://pubmed.ncbi.nlm.nih.gov/1433712/
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CD59 is a GPI-linked membrane protein that inhibits formation of the membrane attack complex of complement. We reported recently that mice have two CD59 genes (termed mCd59a and mCd59b), and that the targeted deletion of mCd59b (mCd59b-/-) results in spontaneous hemolytic anemia and progressive loss of male fertility. Further studies of the reproductive abnormalities in mCd59b-/- mice reported in this study revealed the presence of abnormal multinucleated cells and increased apoptotic cells within the walls of the seminiferous tubules, and a decrease in the number, motility, and viability of sperm associated with a significant increase in abnormal sperm morphologies. Both the capacitation-associated tyrosine phosphorylation and the ionophore-induced acrosome reaction as well as luteinizing hormone, follicle-stimulating hormone, and testosterone serum levels were similar in mCd59b-/- and mCd59b+/+. Surprisingly, the functional deficiency of the complement protein C3 did not rescue the abnormal reproductive phenotype of mCd59b-/-, although it was efficient in rescuing their hemolytic anemia. These results indicate that the male reproductive abnormalities in mCd59b-/- are complement-independent, and that mCd59 may have a novel function in spermatogenesis that is most likely unrelated to its function as an inhibitor of membrane attack complex formation.
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OBJECTIVE: To report a case of hemolytic anemia and methemoglobinemia developing after rasburicase administration to a patient with glucose-6-phosphate dehydrogenase (G6PD) deficiency. CASE SUMMARY: A 50-year-old African American man was hospitalized with new onset seizure, diabetic ketoacidosis, respiratory failure, and acute renal failure. Serum uric acid concentrations were elevated, and the patient was treated with one dose of intravenous rasburicase 22.5 mg for acute renal failure secondary to hyperuricemia. Routine arterial blood gas analyses performed after rasburicase was administered revealed elevated methemoglobin concentrations, which peaked at 14.7%. Hemolytic anemia developed as evidenced by a fall in blood hemoglobin from 14.8 to 5.3 g/dL. The patient made a full recovery following aggressive fluid therapy, blood transfusions, and respiratory support. G6PD deficiency was subsequently confirmed. The Naranjo probability scale indicated that rasburicase was a probable cause of hemolytic anemia and methemoglobinemia. DISCUSSION: Rasburicase is contraindicated in patients with G6PD deficiency as it may cause hemolytic anemia and methemoglobinemia. As of September 26, 2005, simultaneous occurrence of hemolytic anemia and methemoglobinemia has not been reported in patients receiving rasburicase. CONCLUSIONS: As of September 26, 2005, screening for G6PD deficiency should be performed whenever possible prior to chemotherapy administration in patients at risk of developing tumor lysis syndrome.