Abstract
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a genetic X-linked recessive disorder that results from mutations in the G6PD gene, which provides instructions for manufacturing the G6PD enzyme. G6PD deficiency primarily impacts red blood cells. This deficiency can result in hemolytic anemia (HA), in which rapid destruction of red blood cells occurs due to the vulnerability of erythrocytes to reactive oxygen species. It is most commonly found in males and affects 1 in 10 Black males in the United States. Persons with G6PD deficiency may exhibit symptoms such as pallor, jaundice, dark urine, fatigue, tachycardia, shortness of breath, and splenomegaly. Exposure to certain medications such as rasburicase, sulfonamides, nitrofurantoin, antimalarials, dapsone, chloramphenicol, high-dose aspirin, methylene blue, and phenazopyridine may trigger a hemolytic crisis in those with G6PD deficiency. Tests used in the diagnosis of HA include the Coombs test, haptoglobin, complete blood count, urinalysis, lactate dehydrogenase, bone marrow tests, and a peripheral blood smear. This article summarizes the case of a patient who developed HA after an infusion of rasburicase and offers management strategies.
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