RESUMEN
Glucose-6-phosphate dehydrogenase deficiency (G6PD) is the most common enzyme deficiency. Mode of inheritance is X-linked recessive with a high prevalence in endogamous marriages, such as Jehovah's Witness. Oxidative triggers such as infection, ingestion of certain medications, certain types of food, and in rare instances diabetic ketoacidosis (DKA) may unmask the diagnosis by triggering a hemolytic event. We describe the case of a 43-year-old male with type 2 diabetes who presented with DKA and subsequently became anemic four days after his admission, with the hemoglobin continuing to fall. After extensive workup, it was found that the patient had G6PD confirmed by a low glucose-6-phosphate dehydrogenase assay. We hypothesized that the oxidative stress from the DKA unmasked G6PD induced hemolysis in our patient. During our literature search, we also noticed that hemolysis was delayed on average by four to seven days in these patients after the initiation of insulin therapy similar to our patient. It is postulated that the delayed onset of hemolysis may be due to high levels of glucose in the blood. Hyperglycemia may offset the effects of G6PD deficiency by increasing the production of G6PD. When the levels of glucose start falling, hemolysis becomes apparent.