Evaluation of Low Mean Corpuscular Volume in an Apheresis Donor Population.
Authors: Bryant Barbara J. , Hopkins Julie A. , Leitman Susan F. 
Published: April 2020

Donors of apheresis blood components are routinely evaluated with a complete blood count (CBC) at the time of each donation. In otherwise healthy donors, recurrent low mean corpuscular volume (MCV) values (&lt; 80 fL) in the presence of an acceptable hemoglobin (≥ 12.5 gm/dL) could be due to iron deficiency or to an hemoglobinopathy, such as alpha thalassemia trait or a beta chain variant trait. Iron deficiency in repeat blood donors may warrant treatment with oral iron supplementation, whereas donors with hemoglobinopathies in the absence of iron deficiency do not need treatment. Pre-donation samples for CBC (Cell-Dyn 4000, Abbott) were obtained from all apheresis donors donating platelets, plasma, granulocytes, lymphocytes, and monocytes. MCV values &lt;80 fL were electronically flagged via a donor database module for review by medical staff. Donors with MCV ≤ 80 fL on two or more occasions were evaluated for iron deficiency and the presence of hemoglobinopathies. CBC, ferritin, serum iron, transferrin, percent transferrin saturation, and hemoglobin electrophoresis were performed at the time of a subsequent donation. Iron deficiency was defined as values below the reference range for ferritin or transferrin saturation. Alpha thalassemia trait was presumed if the red blood cell count was elevated, no variant hemoglobins were detected by electrophoresis, and the ferritin, percent transferrin saturation, serum iron, and transferrin levels were all within normal ranges. In a one-year period, 25 of 1333 healthy apheresis donors had a low MCV on more than one occasion. Donors with low MCV were more likely to be African American (AA) (12 of 25, 48%) or Asian (2 of 25, 8%) compared with donors without a low MCV (AA 193 of 1308, 15%; Asian 37 of 1308, 3%). Iron deficiency was present in 60% (15 of 25) of the low-MCV donors: 36% (9) had isolated iron deficiency, 20% (5) had iron deficiency with probable alpha thalassemia trait, and 4% (1) had hemoglobin C trait with coexistent iron deficiency. Hemoglobinopathy without concomitant iron deficiency was found in 40% (10 of 25) of the low-MCV donors and included 24% (6) with presumed alpha thalassemia trait, 4% (1) with hemoglobin S trait and single gene deletion alpha thalassemia trait (hemoglobin S concentration 34%), 4% (1) with hemoglobin S trait and double gene deletion alpha thalassemia trait (hemoglobin S concentration 28%), 4% (1) with hemoglobin Lepore trait, and 4% (1) with hemoglobin G-Philadelphia trait with at least a single gene deletion alpha thalassemia trait (hemoglobin G-Philadelphia concentration 36%). Although the combination of MCV, hemoglobin, and red cell count available from the routine CBC were often helpful in discriminating iron deficiency from hemoglobinopathy, the frequent coexistence of both processes resulted in a need for further laboratory evaluation, both before and after iron repletion, to confirm the diagnosis. In a sample of American repeat apheresis donors, iron deficiency is present in the majority with recurrent low MCV values and hemoglobin levels ≥ 12.5 gm/dL. Concurrent hemoglobinopathy is also commonly present but may not be easily recognized in the setting of iron deficiency. The MCV is a useful screening tool to detect iron deficiency in a repeat blood donor population, however low MCV values should be further investigated in the blood donor setting to determine if iron replacement therapy is indicated.