<p>Post-Transfusion Purpura: Current Perspectives</p>

Abstract

Post transfusion purpura (PTP) is an uncommonly reported post transfusion adverse event that can present with severe thrombocytopenia; sometimes resulting in significant bleeding and hemorrhage. Its diagnosis can be elusive given its substantial symptomatic overlap with other thrombocytopenic syndromes. Underdiagnosis and underreporting make the true incidence of disease difficult to define. While clinical suspicion is key, laboratory evidence of platelet-targeted antibodies and identification of the antigen(s) they recognize are necessary to confirm the diagnosis. A curious aspect of PTP is paradoxical destruction of both transfused and autologous platelets. Although the first case was reported over 50 years ago, this aspect of PTP pathogenesis is still not fully understood and is widely debated. Several theories exist, but conclusive evidence to support most is lacking. Despite limited understanding of disease incidence and etiology, treatment with IVIG (Intravenous Immunoglobulin) has become standard practice and can be highly effective. Although recurrence is rare, precautions should be taken if patients with a history of PTP require transfusions in the future.

Characterization of glycoprotein IIb/IIIa‐specific alloantibodies induced by cross‐strain platelet immunization in mice

“…In 80% to 90% of cases, these antibodies are specific for HPA-1a (Pl A1 , Zw a ) encoded by leucine 33 in GPIIIa. 4 Of the remainder, about two-thirds recognize other single AA polymorphisms in GPIIb/IIIa. 17 Thus, 90% to 95% of the platelet-specific alloantibodies found in patients with PTP recognize GPIIb/IIIa.…”

“…The mouse model resembles the human disorder posttransfusion purpura (PTP), in which profound, often lifethreatening thrombocytopenia develops in conjunction with the alloimmune response against a transfused human platelet alloantigen (HPA), usually HPA-1a, defined by a proline to leucine substitution at position 33 of platelet glycoprotein (GP) IIIa. [2][3][4] A long-standing question that has puzzled clinicians and investigators ever since PTP was first described 5 is how an alloantibody incapable of reacting with autologous platelets might nonetheless cause profound thrombocytopenia. Findings made in individual patients with PTP [6][7][8][9][10][11][12] have hinted at the possibility that platelet destruction may actually be caused by a platelet-specific autoantibody that is usually overlooked in serologic studies because it is dominated by the much more potent alloantibody.…”

“…With certain strain combinations, intraperitoneal (IP) immunizations also induced platelet‐reactive autoantibodies and severe thrombocytopenia. The mouse model resembles the human disorder posttransfusion purpura (PTP), in which profound, often life‐threatening thrombocytopenia develops in conjunction with the alloimmune response against a transfused human platelet alloantigen (HPA), usually HPA‐1a, defined by a proline to leucine substitution at position 33 of platelet glycoprotein (GP) IIIa 2–4 …”

Convalescent Plasma in COVID-19. Mortality-Safety First Results of the Prospective Multicenter FALP 001-2020 Trial

“…In patients with COVID-19 especially, it is difficult to assign with certainty the occurrence of TRALI or Transfusion-associated circulatory overload (TACO) since, in the context of mostly severe cases, respiratory failure is the predominant dysfunction and concomitant but potentially unrelated worsening may occur close to the transfusion. As for thrombocytopenia, post-transfusion purpura is rare, with an incidence of less than 0.01%, associated with the detection of antiplatelet antibodies ( 36 ). In the only case of thrombocytopenia, the antiplatelet antibody test was negative.…”

Platelet antibodies in immune thrombocytopenia and related conditions

“…However, for a limited period of time, their autologous platelets are apparently rapidly eliminated through an immune mechanism. Although first cases of PTP were described 60 years ago [66,67], the pathophysiology of this reaction is still not fully understood [68]. Serologic and clinical findings are paradoxical: during a secondary immune response, patients' B-cell-related immune response shows aspects of autoimmunity.…”