Although glucose-6-phosphate dehydrogenase (G6PD) deficiency is less known in Western countries than in the Middle East and Africa, global migration and immigration are bringing ethnic groups with the highest incidence of this inherited genetic disorder into the US healthcare system. The G6PD enzyme is critical to protecting erythrocytes against oxidative stress, and deficiency may lead to hemolysis in the presence of certain environmental factors such as infection and some medications and foods. Neonatal jaundice, favism, and hemolysis are associated with exposure to increased oxidative stressors in patients with G6PD deficiency. By recognizing the potential for G6PD deficiency, clinicians can screen for the disorder and teach affected patients how to avoid triggers that result in harmful clinical manifestations.
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Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a well-known red blood cell enzymopathy and a cause of intravascular hemolysis. This case report presents a child with underlying G6PD deficiency who experienced an acute episode of extensive intravascular hemolysis induced by a scrub typhus infection. The key takeaway from this report is that scrub typhus infection can trigger extensive hemolysis in patients with even "mild" G6PD deficiency, and normal G6PD levels found during the acute phase of hemolysis do not rule out the possibility of underlying G6PD deficiency.
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