T R A N S F U S I O N Volume 28 September-October 19 8 8 Number 5

Editoriuls

ABO blood groups and platelet transfusion

The clinical result of transfusing red cells from group A or B donors into patients with antibodies to those antigens is predictably disastrous. Therefore, there is strict adherence to ABO compatibility in the practice of red cell transfusion. Platelets, however, are generally transfused without regard for ABO compat- ibility. Yet there is a series of papers in the literature suggesting that ABO matching can improve the re- sponse to platelet transfusion, at least in some pa- tients. The article by Skogen et al.1 in this issue de- scribing two group 0 patients who were refractory to platelets from group A, donors but responded well to platelets from group 0 or group A, donors is the latest in this series.2-6 Perhaps it is appropriate to re- view the ABO serology of platelets and comment on our current practice.

The ABH blood group system is not simple. Red cell ABH antigens are located on intrinsic membrane gly- colipids and glycoproteins while their plasma coun- terparts are located predominantly on glycolipids. There are two main types of precursor oligosaccha- ride chains, type 1 and type 2, differing only in the carbon-to-carbon linkage between the terminal galactose and subterminal N-acetylglucosamine. Fu- cose is added to the galactose to form H substance. A and B antigens are formed by the further addi- tion of N-acetylgalactosamine and galactose, respec- tively, to the terminal galactose. ABH antigens in plasma are found predominantly on type 1 chains while those intrinsic to the cell membrane are found predominantly on type 2 chains. The A, and A2 sub- types differ in the number of A sites per cell, pre- sumably because of differences in the substructure of the oligosaccharide chains proximal to the subtermi- nal N-acetylglucosamine. It has been recognized for many years that platelets express ABO antigens, but their nature has been debated. Like red cells, group 0 platelets can adsorb plasma blood group substances’ and it has been proposed that adsorbed antigen ac- counts for all of the antigenic activity. More recently, however, Dunstan et a1.8 used a monoclonal antibody to demonstrate type 2 chains on platelets, providing presumptive evidence that the antigens are as intrin- sic to the platelet membrane as they are to the red cell membrane. They concluded that ABO antigens

on platelets consisted of intrinsic type 2 chains and passively adsorbed type 1 chains in approximately equal amounts. A direct consequence in transfusion practice would be that type 0 platelets pooled with A platelets would adsorb A substance as they await transfusion. At 22OC, adsorption occurs in approxi- mately 40 minutes.’ Therefore, considering the fre- quency of platelet transfusion in the United States? millions of units of antigen-bearing platelets are trans- fused annually into recipients with antibody to that antigen.

Most platelets are transfused as pools of random donor units. To my knowledge, there is no data in the literature that considers whether ABO compati- bility should be observed when pools are prepared or when choosing the units to be pooled for administra- tion to a specific recipient. The data we do have are from transfusions of platelets from single donors. In 1965, Aster transfused Chromium-5 1 -labeled group A, platelets into normal group 0 volunteers and found that in vivo recovery was reduced to one third of that seen with ABO compatible transfusions? The lowest recoveries were seen in recipients with high isoagglu- tinin titers. In 1968, Pfisterer, Thierfelder, and Stich3 confirmed these results with Chromium-5 1 -labeled transfusions in normal recipients. In 1979, Duquesnoy et al.4 found a 23 percent reduction in in vivo recov- ery when platelets from histocompatible donors were transfused into alloimmunized thrombocytopenic re- cipients if the donor typed for group A, B, or both and the recipient did not. They concluded that this reduction in recovery was not great enough to con- traindicate ABO-mismatched transfusions. In 1987, Heal, Blumberg, and MaseF described a 41 percent reduction in recovery in the same clinical setting when group A or B platelets were given to recipients who lacked these antigens. An intriguing aspect of their report was that there was an intermediate degree of reduction in recovery, 18 percent, when the donor plasma contained ABH antibodies to the recipient’s platelets. The authors concluded that this new finding required confirmation, but speculated on the role of soluble ABH antigen in the recipient in producing this result. In all of these reports, there was considerable variability in recoveries among donor-recipient pairs.

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402 EDITORIAL TRANSFUSION VOI 2x. NO s- isxn

Brand et al.5 and Skogen et a1.I reported on extreme examples of the deleterious effect of ABO antibodies in selected patients in this setting. ABO-mismatched transfusions are often very effective clinically, how- ever. At present, there is no explanation for this vari- ability, although studies of the titers and subclasses of ABO antibodies in these patients would be of interest.

It is likely that the practice of single-donor platelet transfusion will remain empiric in the foreseeable future. Both ABO and HLA-A,B should be con- sidered in donor selection, and the fact that many ABO-mismatched transfusions will be effective clini- cally should be recognized. The implications of these results for transfusions of pools from random donors is less clear. Most transfusions are less effective than they should be. In a recent study of a large group of leukemic patients,1° the mean corrected count in- crement was 10.5 X lo9 per 1 per m2 body surface area per unit of platelets transfused. Our knowledge of platelet kinetics and volume of distribution suggests that the increment should be twice that. Among the many factors involved,1° ABO incompatibility may be playing a role in reducing transfusion efficacy. Furthermore, in terms of recipient safety, there are well-documented instances of severe hemolysis due to isoagglutinins present in group 0 platelet concen- trates transfused to group A and group B recipients." In my field of greatest interest, platelet storage, we go to great lengths in terms of plastic bag composi- tion and modes of agitation to achieve 10-20 percent increases in in vivo recovery, thereby improving the efficacy of transfusion. To increase safety, the dura- tion of storage was recently reduced from 7-5 days because of reports of sepsis in recipients. Consider- ing the number of platelet transfusions given each

year, these events were infrequent. It is appropriate to take steps to optimize the efficacy and safety of transfusion therapy. Perhaps we should study the role of ABO compatibility in platelet transfusion therapy more carefully so that further improvements may be made.

SCOTT MURPHY, MD Thomas Jefferson University

Philadelphia, PA

References 1. Skogen B, Rossebo Hansen B, Husebekk A, Havnes T, Hannes-

tad K. Minimal expression of blood group A antigen on throm- bocytes from A2 individuals. Transfusion 1988;28:456-9.

2. Aster RH. Effect of anticoagulant and ABO incompatibility on recovery of transfused human platelets. Blood 1965;26732-43.

3. Pfisterer H, Thierfelder S, Stich W. ABO Rh blood groups and platelet transfusion. Blut 1968;17:1-5.

4. Duquesnoy RJ, Anderson AJ, Tomasulo PA, Aster RH. ABO compatibility and platelet transfusions of alloimmunized thrombocytopenic patients. Blood I979;54:595-9.

5 . Brand A, Sintnicolaas K, Claas FHJ, Eernisse JG. ABO anti- bodies causing platelet transfusion refractoriness. Transfusion 1986;26:463-6.

6. Heal JM, Blumberg N. Masel D. An evaluation of crossmatch- ing, HLA, and ABO matching for platelet transfusions to re- fractory patients. Blood 1987;70:23-30.

7. Kelton JG, Hamid C, Aker S, Blajchman MA. The amount of blood group A substance on platelets is proportional to the amount in the plasma. Blood 1982;59:980-5.

8. Dunstan RA, Simpson MB, Knowles RW, Rose WF. The origin of ABO antigens on human platelets. Blood 1985;65:615-9.

9. McCullough J, Steeper TA, Connelly DP, Jackson B, Hunting- don S, Scott EP. Platelet utilization in a university hospital. JAMA 1988;259:2414-8.

10. Bishop JF, McGrath K, Wolf MM, Matthews JP, De Luke T, Holdsworth R, et al. Clinical factors influencing the efficacy of pooled platelet transfusions. Blood 1988;7 1:383-7.

11. Pierce RN, Reich LM, Mayer K. Hemolysis following platelet transfusions from ABO-incompatible donors. Transfusion I 9 85 ;25 :60-2.