Hemolysis in glucose-6-phosphate dehydrogenase (G6PD) deficiency varies by mutation status and the oxidative stressor. Although classified by percent of enzymatic deficiency, variability in normal G6PD values clouds assessment of hemolysis risk by level. This was a retrospective, single institution, cohort study assessing risk of postexposure medication-induced hemolysis in G6PD deficient patients. Exposures occurred in 87 of 1415 deficient patients. Only 2 of 87 medication-exposed patients had hemolytic episodes and both had very low enzymatic activity. No hemolytic events occurred with G6PD levels >7 units/g hemoglobin. Correlation of levels with mutation may improve predictive capacity for hemolysis in G6PD deficiency.
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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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