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Severe thrombocytopenia in a patient following liver transplantation caused by HPA‐1a antibodies produced by the liver donor

The patient was a 59 y/o male with HCV-associated cirrhosis and HIV, who received a living donor liver transplant in 2016. The patient’s blood type was group A, Rh (D) positive, with a negative RBC antibody screen. In the perioperative period, the patient received 7 units RBC, 9 units plasma, 7 units platelets and 4 pools of cryoprecipitate. He received an additional 1 RBC unit, 8 units of plasma, 2 units of platelets and 1 unit of cryoprecipitate in the postoperative period. Nine days after transplantation, he was readmitted with ecchymosis on his right upper inner thigh and a right arm hematoma and found to have acute kidney injury, edema, ascites drainage and severe thrombocytopenia. The patient’s blood counts included: platelets 7000/lL; WBC 13 300/lL and hemoglobin 16.5 g/dL. The blood smear showed thrombocytopenia and a normochromic, normocytic anemia with increased polychromasia and increased anisocytosis (Figure 1). There was no morphologic evidence of microangiopathic process. The prothrombin time was 12.6 seconds (normal range 9.2 to 13.0 seconds); INR 1.2; aPTT 24.3 seconds (normal 24.6 to 37.4 seconds). The patient’s platelet count was in the 20 000–40 000/lL range at original presentation and in the immediate post-transplant period. The HIV viral load was reported to be less than 20 copies/mL by HIV quantitative real-time PCR. His medications included: methylprednisolone, mycophenolate mofetil, prednisone, tacrolimus, emtricitabine, raltegravir, valganciclovir, piperacillin-tazobactam, and sulfamethoxazoletrimethoprim. In the post-transplant setting, severe thrombocytopenia can be caused by myelosuppression due to medications, idiopathic immune thrombocytopenia, immune thrombocytopenia associated with HCV and HIV infection and hypersplenism. When there is an acute and severe fall in the platelet count, post-transfusion purpura should be considered. Thrombocytopenia seen in hemolytic-uremic syndrome, myelosuppression, and disseminated intravascular coagulation can be ruled out by clinical history and laboratory findings. The platelet count reached a nadir of 3000/lL on the tenth day and was less than 10 000/lL for the next 4 days (Figure 2). Platelet transfusion yielded very low and transient platelet increments during this time. When the platelet count is responding poorly to repeated transfusions, immune thrombocytopenia should be considered. Among treatments for immune thrombocytopenia, intravenous immune globulin (IVIG) most frequently gives a rapid response. The patient was given 4 doses of IVIG, 0.5 g/kg IV daily (on days 10–13), with no response in his platelet counts (Figure 2). Immune suppressive measures include use of high dose corticosteroids. He was then given a 5 day course of methylprednisolone, 125 mg on days 13–17. The patient’s platelet count recovered steadily and returned to normal by the 28 postoperative day. The resolution of thrombocytopenia with immune suppressive therapy lead to an investigation into the immune nature of the severe thrombocytopenia. Because the patient presented with severe thrombocytopenia 9 days after transplantation and blood product exposure, post-transfusion purpura was considered and laboratory tests were ordered. The solid phase platelet antibody screen (Capture-P, Immucor, Inc., Norcross, GA) and the HLA antibody screen were negative on the second day of admission (day 10 after transplantation) (Figure 2). Also, no platelet-reactive antibodies were detected by flow cytometry. The HLA antibody screen performed by Luminex FlowPRA® Class I screening test was negative.