Monoclonal versus polyclonal anti-D in the treatment of ITP

Alan H Lazarus1

  • 1University of Toronto, Department of Laboratory Medicine and the Keenan Research Centre in the Li Ka Shing Knowledge Institute of St. Michael's Hospital, The Canadian Blood Services, Departments of Medicine and Laboratory Medicine & Pathobiology , 30 Bond St, Toronto, Ontario, M5B 1W8 , Canada lazarusa@smh.ca.

Immune thrombocytopenia (ITP) is an autoimmune bleeding disorder caused by low numbers of platelets generally due to the production of anti-platelet antibodies. One effective treatment for ITP patients who express the RhD antigen on their red blood cells has been the use of blood donor-derived pooled polyclonal anti-D. Although anti-D has served us well, it needs to be replaced with a recombinant product. While the mechanism of action of anti-D in ITP remains highly speculative, this has not thwarted attempts to replace anti-D with a monoclonal product. Although a single attempt at a monoclonal antibody was not successful in the 1990s for the treatment of ITP, more recent efforts in mouse models of ITP and ITP patients now show that monoclonal antibodies can be successful in ITP. These studies also finally help substantiate the concept that it is unlikely that contaminants in the original donor-derived preparations mediate the major ameliorative activity of anti-D in ITP.

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