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Platelet ABO Compatibility

The term “ABO-compatible” is confusing when thinking about blood components other than RBCs. Red Blood Cell units contain cells carrying the ABO antigens of the donor and plasma carrying soluble ABO antigens and anti-A and anti-B antibodies. The recipient also possesses ABO antigens and antibodies, but in much larger amounts. Group O blood components do not express cellular and soluble A and B antigens, but do contain anti-A and anti-B antibodies, often in higher titer and avidity than in group A or B components. Group O (so-called universal donor) RBCs usually can be safely transfused to group A or B patients, because the volume of residual incompatible plasma (30 – 70 mL) is minimal. In contrast, a single donor (apheresis) platelet or a pool of 10 random donor platelet concentrates is suspended in 200 to 600 mL of donor plasma. If these platelets are not ABO identical, large volumes of incompatible plasma will be infused, often on a daily basis for extended periods. Anti-A and anti-B can bind to RBCs and to soluble A and B antigens. In the latter instance, immune complexes are formed that can initiate inflammation, tissue injury, and immune suppression. Thus, unlike RBC transfusions, there really are no ABO compatible platelet transfusions. Platelet transfusions should be classified as either ABO identical or nonidentical.

The most obvious adverse effect of transfusing ABO nonidentical platelets is hemolysis. The risk of an ABO hemolytic reaction is rare after a single transfusion of ABO nonidentical platelets, but increases significantly when large volumes are transfused over a relatively short time period. Hemolysis is unlikely after a single ABO incompatible unit for two reasons. First, transfused plasma is diluted almost 10 fold in the patient’s intravascular blood volume. Second, and perhaps most importantly, transfused anti-A and anti-B antibodies are rapidly neutralized by binding to circulating soluble A and B antigens as well as tissue A and B antigens. Transfusion of platelets containing large volumes of ABO incompatible plasma saturates soluble and tissue ABO antigen sites and permits binding of excess anti-A and/or anti-B to red blood cells. When this happens, patients develop a positive direct antiglobulin test (DAT) and possibly hemolysis.

Other serious adverse consequences of transfusing ABO nonidentical platelets have also been reported. Chronically transfused patients with hematologic disease who are transfused with nonidentical ABO platelets achieve lower post-transfusion platelet counts, require almost twice as many platelet transfusions, and develop platelet refractoriness earlier than patients receiving ABO identical platelet transfusions. Transfusion of group A or B platelets to group O recipient results in post-transfusion platelet increments that are 20% less than those obtained with ABO identical platelet transfusions. Decreased platelet survival is due to the binding of recipient anti-A and/or anti-B to the transfused donor platelets. Transfusion of group O platelets to group A or B recipients results in even lower post-transfusion platelet increments, suggesting that incompatible plasma is an even more important risk factor. In this situation, anti-A and anti-B in the transfused plasma forms immune complexes with soluble A and/or B antigens circulating in the recipient’s plasma. These complexes circulate for hours to days after incompatible transfusions and can bind to platelets resulting in their activation and premature destruction.

Transfusion of ABO nonidentical platelets to transplant patients can have even more deleterious effects. Patients receiving allogeneic marrow or stem cell transplants and patients receiving chemotherapy for acute leukemia have increased mortality due to multi-organ failure and sepsis if they are transfused with ABO nonidentical platelets. ABO antigens, like HLA antigens, are widely expressed on the endothelium lining of blood vessels. Anti-A and/or anti-B antibodies present in ABO incompatible platelets appear to inflict direct damage to organs by binding to endothelial A and B antigens. The formation of anti-A and/or anti-B immune complexes also suppresses cellular immunity, resulting in a predisposition to infection.

Apheresis platelets are preferred over random donor platelets, because of the lower risks associated with a decreased number of donor exposures. If ABO identical apheresis platelets are not available, it is most important to avoid transfusing substantial amounts of anti-A and/or anti-B to patients expressing those antigens. Therefore, the second best choice is to provide random donor ABO identical platelets with a bedside leukocyte reduction filter. When neither apheresis nor random donor ABO identical platelets are available, the ordering physician should be consulted to see if the transfusion could be delayed until ABO identical platelets become available. If immediate transfusion is necessary, the following list can be consulted for additional choices.

  • 1st choice is ABO identical apheresis platelet
  • 2nd choice is ABO identical random donor platelets with bedside leukocyte reduction filter
  • 3rd choice is to see if transfusion can be delayed until ABO identical platelets become available
  • 4th choice is ABO nonidentical apheresis platelet (see table above)
  • 5th choice is ABO nonidentical random donor platelets with bedside leukocyte filter

The Transfusion Service should also refrain from infusing substantial amounts of soluble or cell associated A and/or B antigens to patients with detectable levels of the corresponding antibody. The most common example is the transfusion of Group A or B platelets to a group O recipient. This practice is permissible if a patient is hemorrhaging and has a platelet count below 100,000 and neither group O random nor single donor platelets is available.


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