RBC Indices in G6PD Deficiency
During baseline (non-hemolytic) states, G6PD deficiency typically presents with normal RBC indices, as the enzyme defect does not affect red cell size or hemoglobin content when cells are not under oxidative stress. 1
Baseline Hematologic Profile
Between hemolytic episodes, patients with G6PD deficiency have completely normal complete blood counts with normal MCV, MCH, and MCHC. The enzyme deficiency itself does not cause chronic anemia or alter red cell morphology in the absence of oxidative triggers. 1
During Acute Hemolytic Crisis
When exposed to oxidative stressors (fava beans, infections, or certain medications), the RBC indices change dramatically:
- Normocytic normochromic anemia is the characteristic finding during acute hemolysis 1
- Reticulocytosis develops as the bone marrow responds to hemolysis, typically appearing 24-72 hours after oxidative exposure 1
- Heinz bodies (denatured hemoglobin precipitates) appear on peripheral smear during active hemolysis 1
- Hemoglobin levels can drop significantly, sometimes requiring transfusion if below 7-8 g/dL with symptoms 2
Critical Diagnostic Pitfall
Never test G6PD enzyme levels during or immediately after acute hemolytic episodes, as reticulocytes and young RBCs contain near-normal enzyme levels, potentially masking the deficiency. 3 Wait at least 50 days after RBC transfusion before performing enzyme assays, as even 6-12% donor RBC contamination causes false-negative results. 3
Coexistent Conditions That Alter Indices
When G6PD deficiency coexists with other hereditary RBC disorders, the indices change:
- Microcytosis (low MCV) occurs when α-thalassemia is coinherited, found in 65% of G6PD patients with microcytosis 4
- Hereditary spherocytosis coexistence causes more severe anemia with significantly lower hemoglobin, PCV, MCV, and MCH 4
- Patients with all three defects (G6PD deficiency, hereditary spherocytosis, and α-thalassemia) have the most severe phenotype with the lowest hematological parameters 4