What is the pathogenesis of posttransfusion purpura?

Updated: Nov 30, 2019
  • Author: Perumal Thiagarajan, MD; Chief Editor: Srikanth Nagalla, MBBS, MS, FACP  more...
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Platelet GP IIb/IIIa is a major antigen in platelets and is polymorphic. Most individuals have leucine at position 33 (PLA1/PLA1 or human platelet alloantigen [HPA]–1a). A small number of individuals, approximately 1-3% of random populations, have proline at position 33.

Homozygotes with proline are termed PLA1-negative (or HPA-1b, PLA2/PLA2). When PLA1-negative patients receive blood products from HPA-1a–positive individuals, they produce an antibody reactive against HPA-1a. This alloantibody destroys the transfused platelets and the patient's own platelets, leading to a severe form of thrombocytopenia that lasts for several weeks and, sometimes, several months.

Posttransfusion purpura typically occurs 10 days following a transfusion. This syndrome can be induced by a small amount of platelets contaminating a red blood cell transfusion or, occasionally, following fresh frozen plasma (FFP) transfusion. The thrombocytopenia responds to intravenous immunoglobulin (IVIG). Other platelet alloantigens are occasionally implicated in posttransfusion purpura.

A population-based study of inpatients aged 65 years and older found that posttransfusion purpura occurred at an overall rate of 1.8 per 100,000 hospital stays. Risk of posttransfusion purpura were significantly higher with platelet-containing transfusions, greater number of units transfused, and underlying health conditions including a history of cardiac arrhythmias, coagulopathy, leukemia, and transplantation. [7]

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