Investigation of whether the acute hemolysis associated with Rh(o)(D) immune globulin intravenous (human) administration for treatment of immune thrombocytopenic purpura is consistent with the acute hemolytic transfusion reaction model.

Abstract:

BACKGROUND:Immune thrombocytopenic purpura and secondary thrombocytopenia patients treated with Rh(o)(D) immune globulin intravenous (human; anti-D IGIV) have experienced acute hemolysis, which is inconsistent with the typical presentation of extravascular hemolysis -- the presumed mechanism of action of anti-D IGIV. Although the mechanism of anti-D-IGIV-associated acute hemolysis has not been established, the onset, signs/symptoms, and complications appear consistent with the intravascular hemolysis of acute hemolytic transfusion reactions (AHTRs). In transfusion medicine, the red blood cell (RBC) antigen-antibody incompatibility(-ies) that precipitate AHTRs can be detected in vitro with compatibility testing. Under the premise that anti-D-IGIV-associated acute hemolysis results from RBC antigen-antibody-mediated complement activation, this study evaluated whether the incompatibility(-ies) could be detected in vitro with a hemolysin assay, which would support the AHTR model as the hemolytic mechanism. STUDY DESIGN AND METHODS:Seven anti-D IGIV lots were tested to determine the RBC antibody identities in those lots, including four lots that had been implicated in acute hemolytic episodes. Hemolysin assays were performed that tested each of 73 RBC specimens against each lot, including the RBCs of one patient who had experienced acute hemolysis after anti-D IGIV administration. RESULTS:Only two anti-D IGIV lots contained RBC antibodies beyond those expected. No hemolysis endpoint was observed in any of the hemolysin assays. CONCLUSION:Although the findings did not support the AHTR model, the results are reported to contribute knowledge about the mechanism of anti-D-IGIV-associated acute hemolysis and to prompt continued investigation into cause(s), prediction, and prevention of this potentially serious adverse event.

journal_name

Transfusion

journal_title

Transfusion

authors

Gaines AR,Lee-Stroka H,Byrne K,Scott DE,Uhl L,Lazarus E,Stroncek DF

doi

10.1111/j.1537-2995.2008.02083.x

subject

Has Abstract

pub_date

2009-06-01 00:00:00

pages

1050-8

issue

6

eissn

0041-1132

issn

1537-2995

pii

TRF02083

journal_volume

49

pub_type

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