Comparing Platelet Compatibility to Red Cell Compatibility Protocols

Review: comparing platelet compatibility to red cell compatibility protocols

S. ROLIH

Between 1971 and 1980, the number of platelet con- Incidence of Alloimmunization From centrates transfused in the United States increased from Transfusion 0.4 to 2.8 million units.1 That number increased to near- Each RBC or platelet transfusion has the potential to ly 5 million in 1987 and continues to increase in the influence the outcome of future transfusions of the 1990s. The increase in platelet transfusions has led to a same products by inducing the formation of alloanti- concomitant rise in the incidence of platelet alloimmu- bodies. For RBC transfusions, in which ABO and D nization. As a consequence, many transfusion services group-compatible units are routinely given, this is not a or blood product providers have developed platelet significant problem. Only 0.3 percent to 1.3 percent of compatibility protocols to select platelet components all RBC transfusion recipients produce alloantibodies, that will have acceptable survival when transfused to although in selected recipient populations, such as alloimmunized patients. Most serologists are familiar patients with thalassemia or sickle cell anemia, the with compatibility tests used to select red blood cells alloimmunization rate may be as high as 30 percent (RBCs) for transfusion. These tests are performed before because of chronic transfusions.2 Overall, decreased sur- transfusion, whether or not alloimmunization has vival of transfused RBCs due to alloimmunization occurs occurred. Platelet compatibility tests, in contrast, are infrequently. Once alloimmunization occurs, premature implemented only after alloimmunization and develop- loss of future transfused RBCs is prevented by the selec- ment of the refractory state. tion of antigen-negative donor RBCs, using relatively rapid and simple crossmatch tests. Purpose of RBC or Platelet Transfusions Many platelet transfusion failures are due to factors RBC transfusions are used to improve the oxygen-car- other than alloimmunization, such as the storage lesion rying capacity of the blood. They are administered most of the platelets transfused, hypersplenism, fever, or infec- frequently to ameliorate the consequences of acute tion. Alloimmunization occurs most frequently in chron- hemorrhage due to trauma or surgical procedures. ically thrombocytopenic patients who are transfused Transfusions are also used when there is considerable with multiple units of platelets for extended periods of underproduction of RBCs (such as in aplastic anemia), time, although there is contradictory data as to whether when the recipient’s own RBCs do not function nor- there is a direct relationship between transfusion dose mally (as in sickle cell anemia) or when the RBCs have and immune response.4 Dutcher et al.5 and Holohan et a greatly diminished life span (as in thalassemia major).2 al.6 report that 40 percent to 70 percent of leukemic RBCs are administered until the patient improves clini- patients become alloimmunized by transfusion with cally and the hemoglobin concentration is considered platelets. Alloimmunization rates are as high as 80 per- adequate. cent to 100 percent in aplastic patients, presumably Platelets are administered to stop or to prevent active because these patients do not receive immunosuppres- bleeding due to thrombocytopenia. Most often, platelets sive therapy, yet are repeatedly transfused with are transfused to patients with severe thrombocytopenia platelets.5,6 Platelet alloimmunization, if it occurs, begins secondary either to neoplastic conditions involving the within the first few weeks of replacement therapy.7 bone marrow or to chemotherapy.3 Occasionally, they Most of the antibodies involved in platelet alloimmu- are given to patients who have normal platelet counts nization and decreased platelet survival are directed but who produce platelets with abnormal function. toward HLA class I antigens. A smaller percentage

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involves antibodies to platelet-specific antigens, and an transfusion, a CCI of 7,500/µL is considered the mini- even smaller percentage against ABH histoantigens. mum. At 18–24 hours, the desired minimum CCI is Making significant reductions in platelet alloimmuniza- 4,500/µL.9,10 When 1- and 24-hour CCIs are at or above tion rates has been difficult for two reasons. First, our the minimums, the outcome of transfusion is considered understanding of platelet antigen-antibody systems and reasonably good. CCIs below the minimum expected their clinical relevance is rudimentary, particularly when value at 1 hour are often used as a criterion for refrac- compared to our understanding of the clinical relevance toriness.3,11 of RBC-related antigen-antibody systems. Second, there Posttransfusion samples are not routinely collected in is no universally accepted platelet compatibility proto- many hospitals in the United States because of poor col or platelet antibody detection procedure. platelet management protocols, staff inconvenience, or staff shortage. Unfortunately, CCIs are therefore not cal- Initiating Compatibility Testing culated for many platelet recipients. Consequently, onset Certain tests are performed to determine RBC com- of the refractory state is often missed and refractory patibility, including ABO/D determination, antibody recipients may continue to receive platelet transfusions screening, and, when necessary, crossmatching using of decreasing benefit. O’Connell et al.12 studied the fea- 8 donor RBCs and recipient serum or plasma. These tests sibility of using a platelet count taken 10 minutes post- are performed before transfusion, hence the descriptive transfusion to calculate the CCI. The advantage of term “pretransfusion tests.” RBC compatibility testing substituting a 10-minute count is that staff are usually still also includes checking previous transfusion records for working with the patient, and are thus available to draw the recipient’s serologic history. If the patient was test- a sample. The data suggest that counts taken at 10 mined previously, results of current tests are compared with utes posttransfusion provide the same information as the those previously recorded, and the decision to transfuse 1-hour count. any RBC product is based on the entire record. The Using CCIs and clinical condition as indicators of poor antiglobulin phase of the crossmatch is required for transfusion response due to platelet alloimmunization is patients with a history of any clinically significant alloan- similar to relying solely on clinical condition and post- tibody, even if the current antibody detection test is neg- transfusion hematocrit values to identify the onset of ative. Blood lacking the implicated antigen(s) is selected RBC alloimmunization. It may be more practical to deter- for transfusion even if RBCs possessing that antigen are mine the onset of platelet alloimmunization by using 8 serologically compatible. rapid, inexpensive platelet antibody screening proce- In contrast to red cell compatibility tests, those for dures, as employed in RBC pretransfusion testing. Such platelets are not initiated until a patient fails to respond tests should not require the strict adherence to a time to two or more successive platelet transfusions, and non- schedule for sample withdrawal and would provide a immunologic mechanisms have been eliminated as the flexible, alternative, analytical tool to 1- or 24-hour post- cause. Transfusion response is evaluated in a manner transfusion platelet counts. However, it must be remem- that accounts for the number of platelets transfused, the bered that while the detection of antibodies to platelets patient’s blood volume, and the patient’s initial platelet can strengthen the diagnosis of refractoriness due to count. This is accomplished by comparing a corrected alloimmunization, it provides no precise correlation count increment (CCI) with an expected minimum since some antibodies are not clinically significant. response. The formula is as follows: Platelet antibody detection is currently an area of intense CCI = (Posttransfusion – pretransfusion platelet count x body interest, and many institutions are developing in-house surface area in M2) platelet antibody detection tests, and three types of tests Number of platelets transfused × 1011 are being marketed commercially. The timing of the pretransfusion platelet count is important when calculating the CCI. If the pretransfu- ABO and D Compatibility sion count is not taken immediately before transfusion, Compatibility between recipient and donor ABO the value used in the calculation may be misleading. groups is always a concern in RBC transfusions—to the The expected minimum CCI is dependent on the time extent that tests to demonstrate ABO compatibility are a interval between the transfusion and the posttransfusion required part of compatibility testing. Transfusion of platelet count. When the count is taken 1 hour after ABO-incompatible blood nearly always leads to rapid

134 IMMUNOHEMATOLOGY, VOLUME 11, NUMBER 4, 1995 Similarities—platelet and red cell serology

intravascular destruction of RBCs due to the presence tional components. Essentially, products for platelet of complement-binding antibodies in the recipient’s transfusion are administered based on compatibility blood, and to the high density of A and B antigens on with only one group of antigens carried on the recipi- RBC membranes. Platelets also express A and B antigens, ent’s platelets. A similar protocol, if applied to RBC but ABO incompatibility does not present the same transfusions, would focus management on providing problem in platelet transfusions, since the antigens are RBCs compatible with only those blood group antibod- only weakly expressed. For years, platelet concentrates ies most frequently encountered following exposure to have been administered without regard to ABO group antigen, for example, Rh antibodies. Once it was sus- and, in general, are judged to have provided adequate pected that a patient had developed an antibody to ABO- hemostasis. Nevertheless, ABO incompatibility plays a compatible random donor RBCs, the patient would be role in decreased platelet survival, and variability of switched to RBCs phenotypically matched for ABO and platelet transfusion outcome may be seen when ABO- Rh, without determining the exact specificity of the incompatible platelets are given to thrombocytopenic causative antibody, without regard to other antigen sys- patients.13-17 The anti-A and/or anti-B titer of the trans- tems, and without crossmatching for compatibility. fusion recipient may be an important variable in deter- Platelet membranes carry Class I HLA antigens, prod- mining the success of an ABO-incompatible platelet ucts of genes at the HLA-A, -B and -C loci. Platelets do transfusion. Differences in platelet recovery at 24 hours not carry Class II HLA molecules, products of HLA-DR, between compatible and incompatible transfusions are -DQ, and -DP locus genes. The density of Class I antigens often minor. With the exception of those patients with expressed on platelets is highly variable. Products of the high levels of hemolytic anti-A and/or anti-B,14 ABO- HLA-C locus are poorly expressed on platelets and gen- incompatible platelets can be administered when ABO- erally are not considered when selecting HLA-compati- compatible platelets are not available. ble platelets for transfusion. Antigens of other HLA locus ABO incompatibility may be of concern when large genes, in particular those of some HLA-B genes, may volumes of ABO-incompatible platelets are administered also be poorly expressed on platelets. Serologically, two because of anti-A and/or anti-B present in the plasma categories of antigenic epitopes occur: (1) private epi- portion of the concentrates that are capable of hemolyz- topes—antigens that are unique to one HLA gene prod- ing recipient RBCs.18-22 uct, and (2) public epitopes—antigens that occur on Consideration of the D antigen status of recipient and more than one HLA gene product.25 The broad HLA donor is important when random-donor platelets are alloimmunization responsible for the refractory state is transfused to females before or during the childbearing usually caused by public epitopes. Alloantibodies to one years. Platelets do not carry Rh antigens, but platelet of the public epitopes can sensitize a patient to a sub- concentrates carry approximately 0.4 mL of RBC con- stantial number of potential donor platelets. The high tamination per unit. The risk of forming anti-D has been polymorphism of the HLA system complicates the pro- shown to be approximately 8 percent after transfusion vision of HLA-A- and -B-matched platelets. With approx- of 80–110 units of random-donor platelets.23 imately 70 antigens to deal with, the probability of finding HLA-identical platelets is low. When HLA-identi- Transfusion of HLA-Matched Components cal platelets are not available, platelets that carry cross- HLA antigens are the most frequent cause of platelet reactive antigens are often substituted. alloimmunization and subsequent refractory state.24 HLA-compatible platelets are effective in only 60 per- Traditionally, once the refractory state due to alloimmu- cent to 70 percent of platelet transfusions.26-28 On some nization is established, HLA-identical or HLA-compatible occasions, HLA-mismatched platelets produce success- platelets are selected for transfusion.25 As mentioned ful transfusion outcomes in alloimmunized recipi- previously, determination of the refractory state is based ents.29,30 These observations indicate that other most often on clinical evaluation of the patient and cal- non-HLA factors contribute to the immune refractory culation of the CCI. Unlike RBC protocols, there are no state. Cases in which platelet-specific antibodies are requirements that platelet transfusion failures be evalu- responsible for refractoriness have only recently been ated using serologic tests for antibody, that antibody described. In a study by Kickler et al.,31 the sera of 293 specificity be identified, or that antibody detection tests thrombocytopenic patients were studied with immobi- be performed periodically before the transfusion of addi- lized platelet glycoproteins IIb/IIIa and Ib/IX. Two per-

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cent of the samples had antibodies to IIb/IIIa, and none ity-purified HLA Class I and platelet glycoproteins had antibodies to Ib/IX, in contrast to 23 percent with IIb/IIIa, Ib/IX, Ia/IIa, and IV.36 HLA antibodies. Such data indicate that the incidence of An alternative commercial assay is a microwell antibodies to platelet-specific antigens carried on gly- enzyme immunoassay that differs from SPRCA assays in coprotein IIb/IIIa (including PlA1, Baka, Bakb, and Pena) the indicator system used to detect antigen-antibody is low. In some patients, the formation of platelet-spe- interactions. This assay is distributed primarily in Europe cific antibodies is transient.32 and has not received FDA approval for sale in the United States at this writing.37 Serologic Antibody Detection Tests In order to detect most HLA and platelet-specific anti- Traditional RBC antibody detection tests, based on bodies, screening panels of 6 to 20 different platelet the principle of hemagglutination, have, as a minimum, samples are recommended. For this reason, platelet anti- included incubation at 37°C and incorporated an body screening is often difficult for transfusion services, antiglobulin phase.8 Such tests are very successful at because such laboratories do not have access to the nec- detecting clinically significant IgG alloantibodies to essary numbers of platelet samples with which to con- blood group antigens carried on RBCs, including those struct adequate platelet antibody screening tests. The that are histoantigens, HLA-related, or RBC-specific. transfusion service often refers the sample to donor col- Newer assay methods, including gel agglutination or lection facilities or specialized reference laboratories solid-phase red cell adherence (SPRCA) assay, are also that have access to typed donor platelets. Recipient designed to meet the requirements for detection of sig- serum or plasma can be screened by the transfusion ser- nificant RBC antibodies active at 37°C, and include an vice until it can be shown that the patient has become antiglobulin phase. Thus, traditional and newer RBC alloimmunized. Specimens from immunized patients antibody detection tests are similar in design. Serum or can then be forwarded to special collection facilities to plasma is mixed with a dilute suspension of RBCs and be crossmatched with HLA-matched or unmatched incubated at 37°C. Following incubation, unbound platelets. globulins are removed by washing with saline or pass- ing the RBCs through a density gradient. Anti-human Crossmatching globulin is used to facilitate detection of antibodies Requirements for RBC crossmatch tests include the bound to RBCs. Thus, RBC antibody detection tests are ability to detect anti-A and anti-B and other clinically sig- performed easily, completed rapidly (approximately 30 nificant RBC antibodies active at 37°C, and at the minutes), require relatively inexpensive equipment, antiglobulin phase. The tests are flexible in design, per- and are cost-effective tools to predict transfusion out- mitting the use of fresh or stored RBCs with fresh or come. In contrast, and until very recently, platelet anti- stored serum or plasma samples. RBC antiglobulin cross- body detection tests, including lymphocytotoxicity, match tests are required only when the patient has a his- immunofluorescence, ELISA, and radioimmunoassay, tory of clinically significant antibody. RBCs selected for have been technically difficult and time consuming transfusion lack the corresponding antigen as deter- (requiring 3–8 hours to complete), have required mined by antigen-typing tests (using known antibodies) sophisticated equipment, and, in some cases, have and by crossmatch. RBC crossmatch tests are generally failed to detect antibodies to all platelet antigen groups. performed in the same manner as antibody detection Further, reagents and controls have been prepared by tests, and provide good specificity, sensitivity, and pre- the user. Therefore, platelet methods have not been dictive values. Many of these criteria are also important employed widely in many transfusion services or donor for platelet crossmatching. centers. In the last decade, however, several manufac- When alloimmunized patients are unresponsive to turers have introduced relatively simple platelet anti- HLA-matched platelets, the next management step body detection tests that are easily adapted to routine could be to provide platelets also matched for platelet- laboratories. specific antigens. Unfortunately, there are not enough One platelet antibody detection test is based on a reagents available yet to routinely type the platelets of SPRCA assay, and is identical to solid-phase assays used blood donors for these antigens. In addition, it is unlike- for the detection of IgG antibodies to RBCs.33–35 ly that patients would have been typed for platelet-spe- Another assay is an ELISA-based assay that uses affin- cific antigens before they become thrombocytopenic.

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For these reasons, some transfusion services have resort- match to select platelets for alloimmunized patients ed to crossmatching, using platelets from family members whose HLA types cannot be determined, such as or blood donors, to provide the most beneficial products. leukemic patients or those who have uncommon HLA To be of any value, a platelet crossmatching procedure types. These authors have also used the assay to screen should be simple in design, be rapid to perform, have the random platelet samples in order to locate potential ability to use both fresh and stored nonviable platelets, donors for serologically difficult patients. The authors and provide good sensitivity, specificity, and predictive point out that crossmatching large numbers of random- values. Rapid, easy performance is necessary in cases of donor platelets for the identification of pheresis donors refractory patients because these patients often will be is helpful in the management of some heavily alloim- compatible with only a low number of platelet donors. munized patients, and may be of particular use for blood Thus, many crossmatches will need to be performed to centers that do not have access to HLA-typed donor find compatible donors. Time-consuming, technically dif- pools. Some workers have suggested that platelet cross- ficult procedures will only delay the provision of com- matching alone may be an adequate means of selecting patible products. Platelet crossmatch tests should be appropriate platelets for transfusion.43,44 capable of detecting antibodies to HLAs, platelet-specific antigens, and ABO blood group system antigens. Stopping Platelet Crossmatching Platelet crossmatching has been instituted in some The antiglobulin RBC crossmatch is required when facilities because of the difficulties in predicting trans- the patient has a history of clinically significant anti- fusion outcomes based on HLA-matching alone, and bodies. Antigen-negative RBCs are selected for transfu- because of the costs to both the patient and the donor sion, even though antibody is no longer demonstrable. in the event of unsuccessful transfusion. Nevertheless, In the case of platelet transfusion, it may be possible to available data suggest that this procedure is underuti- eventually stop crossmatching and return the patient to lized. The sensitivity and specificity of platelet cross- random-donor platelets. In some patients, the titer of matching averages about 80 percent, although in some HLA antibody decreases or becomes undetectable studies the percentage approaches 100 percent.38–40 despite continued transfusion of platelets from random There is no consensus on the best crossmatch test. donors. At this time, recipients can be successfully treat- Methods used include radiolabeled staphylococcal pro- ed with more readily available unmatched random- tein A, radiolabeled antiglobulin, enzyme-linked donor platelet products. In most cases, after becoming immunoassay (ELISA), fluorescence, or SPRCA. undetectable, the antibodies do not reappear and the For refractory patients, the crossmatch is often used increment after transfusion of platelets from random as an adjunct to HLA matching for the selection of donors then remains satisfactory. Lee and Schiffer45 platelets for transfusion, although a number of studies studied levels of lymphocytotoxic antibodies and have indicated a high predictive value even when the responsiveness to random-donor platelet transfusion in donor and recipient are not HLA-matched.41 The report 234 platelet recipients with lymphocytotoxic antibod- of Kickler et al.42 and a simultaneous report by Rachel ies. Seventy (30%) patients had significant falls in anti- et al.43 have indicated that the percentage of platelets body levels during the course of treatment. In 44 found compatible by crossmatch varies widely from patients, these declines occurred after further antigenic patient to patient. Nevertheless, both groups of authors exposure was reduced either because no transfusions found that compatible platelets could be selected for were administered or because only histocompatible patients, even if those patients had lymphocytotoxic platelets were transfused. Thirty-five evaluable patients antibodies to 100 percent of lymphocyte donors, pro- with declining levels of lymphocytotoxic antibodies pre- vided enough crossmatches were performed. In fact, viously refractory to platelet transfusions underwent Kickler et al.42 report that effective platelets could be rechallenge with random-donor platelets. All but one provided by crossmatch methods, even though con- had good responses to these unmatched transfusions for ventional HLA-matching tests would have indicated the 2 weeks to 36 months, and antibody did not return platelets to be unsuitable. O’Connell et al.44 have found despite repeated challenges. cases in which the HLA types of successful single-donor platelets selected by crossmatch differ widely from the Conclusions patient’s HLA type. They have used a solid-phase cross- A variety of data indicate that platelet compatibility

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procedures assist in the selection of optimal products HLA and ABO matching for platelet transfusions to refractory for transfusion. Unfortunately, some platelet compati- patients. Blood 1987;70:23–30. 16. Lee EJ, Schiffer CA. ABO compatibility can influence the results bility protocols are underutilized and lack universal of platelet transfusion: results of a randomized trial. Transfusion application. Some aspects of platelet compatibility pro- 1989;29:384–9. tocols are similar to those for RBC transfusions, includ- 17. Carr R, Hutton JL, Jenkins JA, et al. Transfusion of ABO-mismatched platelets leads to early platelet refractoriness. Br J ing the use of an antiglobulin test for the detection of Haematol 1990;75:408–13. platelet antibodies. In other aspects, platelet and RBC 18. Zoes C, Dube VE, Miller HJ, et al. Anti-A1 in the plasma of compatibility protocols, such as the point in the trans- platelet concentrates causing hemolytic reaction. Transfusion fusion cycle at which tests are initiated, differ. Platelet 1977;17:29–32. 19. McLeod BC, Sassetti RJ, Weens JH, et al. Hemolytic transfusion compatibility protocols are currently receiving much reaction due to ABO-incompatibile plasma in platelet concen- attention, and it is possible that future platelet compat- trate. Scan J Haematol 1982;28:193–6. ibility protocols will resemble RBC pretransfusion pro- 20. Conway LT, Scott EP. Acute hemolytic transfusion reaction due to ABO incompatible plasma in a plateletpheresis concentrate tocols more closely. (letter). Transfusion 1984;24:413–4. 21. Pierce RN, Reich LM, Mayer K. Hemolysis following platelet References transfusions from ABO-incompatible donors. Transfusion 1. Surgenor DM, Wallas EL, Hao SHS, Chapman RH. Collection and 1985;25:60–2. transfusion of blood in the United States, 1982-1988. New Eng 22. Murphy MF, Hook S, Waters AH, et al. Acute haemolysis after J Med 1990;322:1646–51. ABO-incompatible platelet transfusions. Lancet 1990;1:974. 2. Mollison PL, Engelfriet CP, Contreras M. Blood transfusion in 23. Goldfinger D, McGinniss MH. Rh-incompatible platelet transfu- clinical medicine. 9th ed. Oxford: Blackwell Scientific sion—risks and consequences of sensitizing immunosup- Publications 1993;391-4;112;453. pressed patients. N Engl J Med 1971;284:942–4. 3. Tomasulo PA, Petz LD. Platelet transfusions. In: Petz LD, 24. Murphy MF, Waters AH. Immunological aspects of platelet Swisher SN, eds. Clinical practice of transfusion medicine. 2nd transfusions. Br J Haematol 1985;60:409. ed. New York: Churchill Livingstone, 1989:427–87. 25. Kickler TS. The platelet transfusion refractory state: transfusion 4. Slichter SJ. Platelet alloimmunization. In: Anderson KC, Ness practices and clinical management. In: Kurtz SR, Brubaker DB, PM, eds. Scientific basis of transfusion medicine. Implications eds. Clinical decisions in platelet therapy. Bethesda, MD: for clinical practice. Philadelphia: WB Saunders Co., American Association of Blood Banks, 1992;97:89–92. 1994:527–8. 26. Pegels JG, Bruynes ECE, Englefriet CP, von dem Bourne AEGKr. 5. Dutcher JP, Schiffer CA, Aisner J, Wiernik PH. Long-term follow- Serological studies in patients on platelet and granulocyte sub- up of patients with leukemia receiving platelet transfusions: stitution therapy. Br J Haematol 1982;52:59–68. identification of a large group of patients who do not become 27. Duquesnoy RJ, Filip DJ, Rodney GE, et al. Successful transfusion alloimmunized. Blood 1981;58:1007–11. of platelets “mismatched” for HLA antigens to alloimmunized 6. Holohan TV, Terasaki PI, Deisseroth AB. Suppression of trans- thrombocytopenic patients. Am J Hematol 1977;2:219–26. fusion-related alloimmunization in intensively treated cancer 28. Dahlke MB, Weiss KL. Platelet transfusion from donor mis- patients. Blood 1981;58:122–8. matched for crossreactive HLA antigens. Transfusion 7. Kickler TS. Platelet immunology. 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39. Ware R, Reisner EG, Rosse WF. The use of radiolabeled and flu- 43. Rachel JM, Summers TC, Sinor LT, Plapp FV. Use of a solid orescein-labeled antiglobulins in assays to predict platelet trans- phase red blood cell adherence method for pretransfusion fusion outcome. Blood 1984;63:1245–8. platelet compatibility testing. Am J Clin Pathol 1988;90:63–8. 40. Rachel JM, Sinor LT, Tawfik OW, et al. A solid-phase red cell 44. O’Connell BA, Lee EJ, Rothko K, et al. Selection of histocom- adherence test for platelet cross-matching. Med Lab Sci patible apheresis platelet donors by crossmatching random 1985;42:194–5. donor platelet concentrates. Blood 1992;79:527–31. 41. Freedman J, Gafni A, Garvey MB, Blanchette V. A cost-effective 45. Lee EJ, Schiffer CA. Serial measurement of lymphocytotoxic evaluation of platelet crossmatching and HLA matching in the antibody and response to nonmatched platelet transfusions in management of alloimmunized thrombocytopenic patients. alloimmunized patients. Blood 1987;70:1727–9. Transfusion 1989;29:201–7. 42. Kickler TS, Ness PM, Braine HG. Platelet crossmatching: a direct Susan Rolih, MS, MT(ASCP)SBB, Vice President, approach to the selection of platelet transfusions for the alloimmunized thrombocytopenic patient. Am J Clin Pathol Technical Services, Immucor, Inc., 3130 Gateway 1988;90:69–72. Drive, Norcross, GA 30091-5625.

ATTENTION

Red Cross Reference Laboratory Conference. The annual reference laboratory conference will be held on June 7, 8, and 9, 1996, at the Sheraton Reston Hotel, located at Dulles Airport in Reston, Virginia.

If you want to be certain to receive more information about this conference, contact: Delores Mallory, Musser Blood Center, 700 Spring Garden Street, Philadelphia, Pennsylvania 19123-3594, or phone (215) 451-4905, or fax (215) 451-2538.

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