Studies on the pathophysiology of posttransfusion purpura

T. S. Kickler, P. M. Ness, J. H. Herman, W. R. Bell

Research output: Contribution to journalArticlepeer-review

Abstract

Posttransfusion purpura typically occurs in PL(A1) negative blood recipients who have been previously immunized to the PL(A1) antigen. Following transfusion, severe thrombocytopenia develops with the formation of anti-PL(A1). Since the patients' platelets lack the PL(A1) antigen, one would not expect this antibody to destroy autologous platelets. In this study we show that PL(A1) antigen exists in stored blood and can absorb to PL(A1) negative platelets making them PL(A1) reactive. Incubating PL(A1) (-) platelets with ultracentrifuged plasma from PL(A1) (+) blood donors allowed anti-PL(A1) to bind to PL(A1) (-) platelets. Control plasma from PL(A1) (-) blood donors did not lead to anti-PL(A1) binding. Using an inhibition assay, we showed that stored blood contains PL(A1) material that was not removed by ultracentrifugation. The material absorbing to PL(A1) (-) platelets represented the PL(A1) antigen, which was confirmed by Western blotting. After incubating plasma containing PL(A1) antigen with PL(A1) (-) platelets, reactivity at 95,000 D was observed. Native PL(A1) (+) platelets showed a similar band. When PL(A1) (-) platelets were incubated with plasma from a PL(A1) (-) donor, this band was not present. These studies show that a soluble form of PL(A1) antigen exists in stored blood that can absorb to PL(A1) (-) platelets. Consequently, anti-PL(A1) can bind to these platelets leading to thrombocytopenia. These observations may explain the autologous destruction of platelets in posttransfusion purpura.

Original languageEnglish (US)
Pages (from-to)347-350
Number of pages4
JournalBlood
Volume68
Issue number2
DOIs
StatePublished - 1986

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

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