The white cell differential was essentially normal; however, the red cell morphology was abnormal, showing basophilic stippling, slight polychromasia, moderate teardrop cells, and occasional schistocytes and ovalo-cytes.
Pertinent Chemistry Results
Direct bilirubin Total bilirubin Indirect bilirubin SGOT LDH
0.7 mg/dL (0.0 to 0.4 mg/dL) 7.9 mg/dL (0.1 to 1.4 mg/dL) 7.2 mg/dL (0.1 to 0.8 mg/dL) 567 IU/L (0 to 100 IU/L) 2844 IU/L (0 to 100 IU/L)
This case is an example of a patient with G6PD deficiency He has suffered a violent hemolytic episode as a result of exposure to drugs—aspirin in this case. This previously healthy individual has no idea that he has an abnormal G6PD variant. He is very ill, and his red count, hemoglobin, and hematocrit are extremely depressed. Notice that his MCV is macrocytic and his MCH and RDW are also elevated. The indirect bilirubin, SGOT, and LDH are each increased, and these serum chemistry elevations are indicative of a hemolytic episode of monumental proportions.
The MCV is increased due to increased reticulocyto-sis that manifests in the peripheral circulation as poly-chromasia and nRBCs, as seen in this patient's peripheral smear. A Heinz body preparation was performed by allowing equal volumes of EDTA blood to mix with crystal violet stain for 20 minutes. Several Heinz bodies were observed in this preparation. The hemolysis in G6PD deficiency is primarily intravascular as noted by the hemoglo-binuria and hemoglobinemia. However, because most individuals have enlarged spleens, not all of the cell lysis is of the intravascular type; some will be extravascular. Most individuals who have G6PD deficiency remain in a steady state and are hematologically normal; they hemolyze only when exposed to an oxidative drug. Fortunately, for these individuals, these events are self-limiting and, while troubling, their hematological status will return to normal.
110 Part II • Red Cell Disorders
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