Abstract
Transfusion-related acute lung injury (TRALI) is a serious complication of plasma-containing blood components. Studies have implicated HLA antibodies along with biologically active lipids in stored blood in the pathogenesis of TRALI. We reviewed the HLA Antibody testing of our whole blood donors during a three month period who were tested for HLA Class I and HLA Class II antibodies by the DONORSCREEN-HLA Class I and Class II ELISA from GTI Diagnostics @ Waukesha, WI. The testing for HLA Antibodies in our donors was implemented as both HLA Class I and HLA Class II antibodies have been implicated in TRALI. The goal was to quarantine the plasma from these donors in order to reduce the exposure to patients to plasma from HLA Immunized Donors. Of 4056 whole blood donors, there were twenty-two donors of which 21 female and one male who tested positive for either HLA Class I or HLA Class II antibodies whose plasma was transfused. Of the twenty two donors, twenty one were females and one was male. Of the twenty one females, fifteen tested positive for HLA Class I antibodies and seven tested positive for HLA Class II antibodies. The single male donor tested positive for HLA Class II antibodies. The cause of the HLA immunization of these donors was unknown (as to whether they were caused by multiparity or blood transfusions). The plasma from the HLA Immunized female donors were transfused to ten female patients and eleven male patients. The plasma from the male donor was transfused to a male patient. All of the plasma from the HLA immunized donors was pooled with other plasma products in pools ranging from three to eight. All of the plasma products were irradiated and transfused via Fenwal Sepacell Reduction Filter for Red cells and all of the patients were premedicated prior to transfusion. One male and one female patient received plasma on two occasions from two donors both of whom were positive for HLA Class I antibodies. The twenty two patients consisted of four with hematological malignancies, one with a lymphoid malignancy and seventeen with malignancies of solid organs. Three of the patients had received an autologous transplant and one had received an allogeneic unrelated transplant. None of the patients had received IVIG therapy. The transfusions reactions reported for the three months of this review was also reviewed. None of the patient that received the HLA immunized plasma products was reported to have suffered a transfusion reaction. Although we did not meet our goal of reserving 100% of our plasma products from HLA immunized donors as recovered plasma, we discovered that the plasma products that were transfused from the HLA immunized donors were not associated with transfusion reactions in our patient population. The reason for not meeting our goal was the test results for the HLA Class I and HLA Class II antibodies were received after the plasma products were released for transfusion, due to logistical limitations in the performance of the testing. Although the number is small, we feel that the results may be significant in light of the current thinking of accepting only male donors for plasma products.
HLA class II donor specific antibodies are associated with graft cirrhosis after liver transplant independent of the mean fluorescence intensity level