Post-transfusion purpura (PTP) is a rare yet serious disease characterized by severe thrombocytopenia occurring after a blood transfusion. It is caused by alloimmunization against platelet antigens, anti-HPA-1a being the most frequent antibody. We report two cases of PTP and discuss the clinical presentation, diagnosis and management of this serious condition.

Case Report

Case 1) Female patient, 90 years old, Caucasian, had a fracture in the umerus and head trauma in 2012, followed by upper GI bleeding. Four days after receiving two units of packed RBCs, she presented with a low platelet count (14.000/mm3), petechiae, gum bleeding and oozing from venipuncture sites. The platelet count further dropped to 2.000/mm3the following day. HPA genotyping and HPA antibody identification by MAIPA were performed to investigate post-transfusion purpura, which showed: HPA1bb, 3aa, 5aa and 15ab and presence of antibodies anti-HPA-1a. IVig 400 mg/kG was infused in two consecutive days, with normal platelet counts observed after a week. Two of her three children had the same HPA1bb genotype and performed a matched platelet and RBC donation by apheresis. One matched RBC unit was transfused to correct symptomatic anemia caused by bystander hemolysis seven days after the first transfusion. No platelet transfusions were needed.

Case 2) Female patient, 29 years old, afrodescendant, had a hemorrhagic shock after an emergency hysterectomy due to placenta percreta in 2012. She received 14 RBC units, 10 fresh frozen plasmas and 10 units of cryoprecipitate. Two days later, another surgery was necessary to remove a retained coagulum, and she received 10 units of random platelets. Five days later, the platelet count dropped to 5.000/mm3, followed by sudden anemia (Hb=9--> 4,5 g/dL), without clinical or laboratory signs of hemolysis or evidence of bleeding, with normal coagulation times. HPA genotyping and antibody identification by MAIPA were performed and showed an HPA1bb genotype and presence of an anti-HPA-1a antibody. No platelet transfusions were administered and IVig 500mg/Kg was prescribed for 2 days. Only washed RBC units were transfused thereafter. The platelet count rose four days after starting IVig to 134.000/mm3, yet a second course of IVig was necessary a week later to reach normal platelet counts.


Both reports illustrate severe thrombocytopenia in patients who presented with sudden thrombocytopenia up to a week after blood transfusion. Platelet alloimmunization happens after exposure to HPA antigens by transfusion or pregnancy, and severe thrombocytopenia occurs as an anamnestic response after reexposure to platelet antigens in any blood product that contains contaminating platelet membranes. The thrombocytopenia may evolve as an autoimmune process, which may also cause hemolytic anemia due toa bystander phenomenom. Diagnosis is based on the identification of the antibody in the serum of a patient who lacks the corresponding antigen, anti-HPA-1a being the most common. IVig 0,5-1g/Kg for 2 days is the treatment of choice. The RBC units must be washed to avoid exposure to platelet membranes and recurrence of thrombocytopenia. In future transfusions, washed RBCs or HPA1bb blood products should be used.


No relevant conflicts of interest to declare.

Author notes


Asterisk with author names denotes non-ASH members.