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Risk of post-transfusion thrombocytopenia after red cell transfusions in patients with anti-PlA1 (HPA1) |
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A Canadian colleague reports that her hospital is evaluating a potential liver transplant for a teenaged patient who has an anti-platelet antibody with anti-HPA-1a (PLA1) specificity. The patient will likely require red cell transfusion during and/or after the transplant surgery. She thinks that it is unlikely that red cell donors who are HPA-1a (PLA1) negative will be available when required. Fearful of the potential for profound thrombocytopenia after red cell transfusion she is seeking advice on how to provide red cell support in this case. Of note is that 100% of RBC products used in her hospital are leukocyte-reduced, since her hospital relies on the Canadian Blood Services for blood products. She poses the following questions:
ADDENDA Aug 31, 2004 The following responses have been received.
1. Dr. Simon Panzer of the Medical University of Vienna, Clinic for Blood Group Serology (attribution used with permission) reports that in his limited experience of two patients in whom there were DETECTABLE anti-HPA-1a (in contrast to undetectable anti-HPA-1a), neither patient experienced PTP following transfusion therapy. In his opinion, PTP seems to occur when anti-HPA-1a exhibits significant boosting from a non-detectable status following a transfusion episode. Therefore, he feels the risk of PTP in an individual with detectable antibody should be low. In addition, based on his experience, if PTP develops, treatment with IVIG is effective, Finally, he reports that his center is able to obtain HPA-1a matched RBCs and platelets. ADDENDA Sept 6, 2004 2. A transfusion medicine physician in Denmark reports that his group has had one experience with a case of liver transplantation after post-transfusion purpura due to anti-HPA-1a. It is reported that although the patient received multiple transfusions of blood products from random donors (13 units of filtered SAG-M erythrocyte suspension and 23 units of fresh frozen plasma) and the liver donor was HPA-1a positive, there was no recurrence of PTP. Splenectomy was performed in connection with the liver transplantation in order to interfere with possible elimination of platelets. This case has been published in Clin Transplantation 1993:7:253-257. ADDENDA Sept 7, 2004 3. A physician in Amsterdam agrees with Dr. Simon Panzer of the Medical University of Vienna, Clinic for Blood Group Serology (addendum #1 above) that PTP develops as (a secondary) immune response initiating a strong boost of antibody production. Theoretically, the strong initial antibody production might be partly non-specific because of an incomplete restricted immune response. In case of already detectable antibodies, memory and a directed immune response can be expected. In Amsterdam, at the responding colleague's institute, it is reported that some years ago they did see a couple of PTPs each year. Interestingly, since the introduction of leukocyte-reduction (< 10E6, by in line filtration, but also with very few platelets left) they apparently have seen no further cases of PTP being referred to their lab. ADDENDA Sept 8, 2004 4. Dr. Panzer (see addendum #1) wishes to add to this discussion that he his group has had the same experience as the Amsterdam group (see addendum #3), that PTP became extremely rare since all blood products are leukocyte-depleted. He adds that with leukocyte reduction, RBC products became almost devoid of platelets. His experience is further supported by the findings that in their experience 0.3 to 0.5% of individuals receiving platelet support have detectable anti-HPA-1 (more common HPA-1b than -1-a) and about 5 to 10 times more patients have anti-HPA-5. Still PTP does not develop, even if these patients are transfused with 'incompatible' platelet concentrates. Thus, in the presence of detectable antibodies, a platelet transfusion my not result in the expected platelet count increment, but PTP apparently will not ensue. |
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Please submit comments to the e-Network Forum. Ira A. Shulman, MD |
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Posted: August 27, 2004
Addenda:Aug. 31, Sept 6, 7 & 8, 2004 |
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