Post-transfusion purpura (PTP) shares a key immune mechanism with fetal and neonatal alloimmune thrombocytopenia (FNAIT), both involving platelet alloantibodies that cause rapid platelet destruction, according to a chapter on posttransfusion purpura in the fourth edition of the journal Transfusion Medicine and Hemostasis.
PTP is a rare but serious complication following blood transfusion, leading to an abrupt and severe drop in platelet count, often below 10,000 per microliter. It primarily affects individuals previously exposed to foreign platelet antigens, usually through pregnancy or prior transfusions. Without prompt recognition and treatment, PTP can cause life-threatening bleeding, with a mortality rate approaching 10%.
“The patient with PTP presents with unexplained purpuric rash, bruising, or mucosal bleeding 2 to 14 days after transfusion,” said the author of the chapter. She continued, “The disease can be self-limited, and the platelet count usually recovers within 21 days in the absence of treatment.”
The condition arises when the immune system mistakenly attacks the body’s own platelets after exposure to transfused platelet antigens. Most cases involve antibodies against human platelet antigen-1a, which is present in transfused blood products. PTP occurs more frequently in women who have been previously sensitized during pregnancy. Although the incidence is relatively low—approximately 1 in 63,000 transfused components in the United States—delayed diagnosis can lead to serious complications. Symptoms typically emerge within two weeks of transfusion and include unexplained bruising, a purpuric rash, and mucosal bleeding.
Read more about the prognosis of FNAIT
Confirming PTP requires a combination of clinical assessment and specialized laboratory testing. Patients often exhibit large platelets on blood smears, increased megakaryocytes in bone marrow samples, and detectable platelet-specific alloantibodies. Glycoprotein-specific antigen capture assays, enzyme-linked immunosorbent assays, and molecular HPA genotyping help identify the causative antibodies. The time lag between transfusion and symptom onset can complicate diagnosis, leading to initial misclassification as other platelet disorders such as heparin-induced thrombocytopenia or autoimmune thrombocytopenia.
Intravenous immunoglobulin (IVIG) is the primary treatment and is highly effective in about 85% of cases. Patients typically receive 400 to 500 mg/kg daily for five days or 1 g/kg for two days, leading to platelet recovery within three to five days. Corticosteroids alone are generally ineffective, though they may be used alongside IVIG. In cases unresponsive to IVIG, plasma exchange may shorten the duration of thrombocytopenia. For severe bleeding, transfusions of antigen-negative platelets may provide temporary relief, though survival of these transfused platelets can be limited.
“Conclusive data, however, supporting that leukoreduced RBCs contain insufficient platelet antigens to cause PTP are very limited,” explained the author of the chapter.
Long-term prevention strategies remain uncertain. Recurrence of PTP is rare, but some experts recommend transfusing leukoreduced or antigen-negative red blood cells to minimize risk. The potential benefits of universal leukoreduction remain inconclusive, though studies suggest it may reduce PTP cases by decreasing platelet antigen exposure. Patients with a history of PTP should discuss transfusion precautions with their healthcare providers to ensure safer future blood product administration.
Although PTP remains an uncommon complication, early diagnosis and treatment significantly improve outcomes. Increased awareness among healthcare professionals and patients with prior transfusion or pregnancy history is crucial to reducing severe bleeding risks and improving long-term management strategies.
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