A transfusion medicine fellow who is in training at an academic center in California recently evaluated a potential blood donor (of Asian heritage) known to have G6PD deficiency. For reasons other than his G6PD deficiency, the donor did not make a blood donation. In spite of the donor's deferral, the fellow conducted a review of AABB Standards (21st edition) and the Code of Federal Regulations, which she felt yielded no specific guidance on the issue of eligibility of donors with G6PD deficiency. To pursue the question of whether red cells from an otherwise healthy G6PD-deficient donor were safe for transfusion, the fellow did a literature search and found the following articles which she felt were germane to this question:

• McCurdy PR et al. Vox Sang. 1975;28:230-7 (Washington D.C. & Connecticut, USA) The authors stated: "Clinical evaluation of 23 patients who received 24 units of G6PD-deficient blood (G6PD A-) failed to reveal any deleterious effects." The patient charts were reviewed retrospectively. The authors noted that most recipients did not receive drugs known to be hemolytic, and laboratory follow-up was limited, with few chemical measurements of hemolysis.
• Mimouni F et al. Isr J Med Sci. 1986; 22:120-2 described hemolysis in two preterm infants who received G6PD-deficient donor blood. The donors were of Iraqi and Bulgarian origin. Neither infant received drugs known to be hemolytic. Both infants required exchange transfusions due to decreases in hemoglobin and increased bilirubin after simple transfusion of the implicated units.
• Shalev O et al. Vox Sang. 1993;64:94-8 (Israel) reported a prospective longitudinal study comparing 10 adult patients who received 1 unit of G6PD-deficient red cells and 1 unit of normal red cells, with 10 adult patients who received 2 units of age-matched normal red cells. In the recipients of G6PD-deficient blood, the 24 hr serum bilirubin and LDH values were higher than in the recipients of normal units (mean bilirubin 36 vs. 18 micromols/L; LDH 378 vs 264 IU/L). The difference in bilirubin persisted at 48h (26 vs. 14 micromols/L) with a "marginal difference" in LDH.
• Huang C et al. Am J Hematol. 1998;57:187-192 (Taiwan) evaluated 48 adult patients transfused with 1 unit G6PD-deficienct blood and 1 unit normal red cells. The patients were not treated with oxidative medications. The hemoglobin, hematocrit, bilirubin, and haptoglobin levels were not statistically different from recipients of normal RBCs, and the bilirubin and haptoglobin values did not change significantly from before transfusion.

From her review of the above literature she concluded that aside from increased hemolysis in premature infants and chemical changes reflecting mild hemolysis in 1 of the 2 prospective studies in adults, there do not appear to be significant adverse clinical consequences following transfusion of G6PD deficient blood. She wonders what policy (if any) other centers have developed for these donors.

• Are these donors accepted?
• If not, why not and what are the donors told if they are deferred?
• If they are accepted, are there any special precautions taken to avoid transfusing these units to low birth weight infants or to avoid using the donated red cells for exchange transfusion in neonates?
• Has anyone had experience with infants who have had subsequent difficulties related to transfusion of G6PD-deficient donor blood?

The following comments have been received.

ADDENDA May 18, 2004

1. A colleague from Pennsylvania reports that he believes that red cells with G6PD deficiency would not be expected to have an average 100 day lifespan. Shortened red cell survival may also be expected in persons with alpha thalassemia trait and sickle cell trait. Therefore, he will bar these individuals from red cell donation since they are likely to produce a suboptimal product. He will recruit them only for plateletpheresis or plasmapheresis, if their health allows this. (He reports that although donors with sickle cell disease may undergo vaso-occlusive sickle crisis in automated plateletpheresis, he would not deny a plateletpheresis donation from a healthy woman with sickle cell disease whose baby had neonatal alloimmune thrombocytopenia.)

ADDENDA May 24, 2004

2. A retired pediatric hematologist and former ARC Medical Director in Northern California is interested in hearing from blood bankers in countries where there is a preponderance of racial groups known to have an increased incidence of G6PD deficiency - i.e., those around the Mediterranean, in Africa and in Asia. Their experience with donors and recipients, and policies developed from this, should shed more light on this issue than that gained from the opinions of many of us in North America who see comparatively few donors from these groups. He also wonders whether anyone in the above countries screens male donors for G6PD deficiency.

ADDENDA May 27, 2004

3. According to a colleague in the UK, people known to have G6PD deficiency are permanently excluded from giving blood. However, donors are not specifically queried about this genetic condition. For example, donors are not specifically asked this at the donor session. They are asked more general questions like 'Have you been told that you should never give blood'? and 'Have you ever had jaundice'? He adds that it must also be admitted that even if their interview staff was screening a male donor of Afro-Caribbean or Mediterranean origin, the staff would be unlikely to think of ascertaining the possibility of G6PD deficiency. However, as far as the responding colleague knows, they have no direct evidence of any post-transfusion hemolytic reaction in the whole history of transfusion in the UK (over 100 million donations) being due to a donation from a G6PD-deficient donor. He concludes saying "Mollison's text quotes older literature which indicates only slightly reduced viability of G6PD-deficient donor blood on storage, but points out the theoretical risk of such blood when transfused to a recipient on oxidative medications."

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Ira A. Shulman, MD
CBBS e-Network Forum Editor & Moderator