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Blood, 1 August 2006, Vol. 108, No. 3, pp. 943-946.
Prepublished online as a Blood First Edition Paper on April 6, 2006; DOI 10.1182/blood-2005-06-009761.
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HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Brief report
Relative efficacy of intravenous immunoglobulin G in ameliorating thrombocytopenia induced by antiplatelet GPIIbIIIa versus GPIb antibodies
Michelle Lee Webster,
Ebrahim Sayeh,
Min Crow,
Pingguo Chen,
Bernhard Nieswandt,
John Freedman, and
Heyu Ni
From the Canadian Blood Services, Ottawa, ON, Canada; the Toronto Platelet Immunobiology Group, and Department of Laboratory Medicine, St Michael's Hospital, Toronto, ON, Canada; the Department of Laboratory Medicine and Pathobiology, and the Department of Medicine, University of Toronto, ON, Canada; the Institute of Clinical Biochemistry and Pathobiochemistry and Rudolf Virchow Center for Experimental Biomedicine, University of Würzburg, Germany.
Intravenous immunoglobulin G (IVIG) is used to treat idiopathic thrombocytopenic purpura (ITP). Although many patients benefit from IVIG, some are refractory to this therapy. ITP is characterized by platelet clearance mediated primarily by antiplatelet antibodies against GPIIbIIIa and/or the GPIb complex. These 2 groups of antibodies may induce ITP through different mechanisms. We tested the hypothesis that IVIG may not be equally effective in preventing ITP caused by anti-GPIIbIIIa versus anti-GPIb antibodies in mice. Thrombocytopenia was induced in BALB/c mice using monoclonal antibodies against either mouse GPIIbIIIa (JON1, JON2, and JON3) or GPIb (p0p3, p0p4, p0p5, p0p9, and p0p11). Pretreatment with IVIG significantly ameliorated ITP in all anti-GPIIbIIIa–injected animals. Conversely, IVIG failed to prevent ITP in all anti-GPIb–treated mice, except for p0p4. These results were repeated in C57BL/6 mice, and with different IVIG preparations. These data in mice suggest that patients with ITP mediated by anti-GPIb antibodies may be less responsive to IVIG treatment.
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R. S. Go, K. L. Johnston, and K. C. Bruden
The association between platelet autoantibody specificity and response to intravenous immunoglobulin G in the treatment of patients with immune thrombocytopenia
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February 1, 2007;
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283 - 284.
[Abstract]
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