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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. This Article Full Text (PDF) All Versions of this Article: blood-2005-06-009761v1 108/3/943    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Webster, M. L. Articles by Ni, H. Search for Related Content PubMed PubMed Citation Articles by Webster, M. L. Articles by Ni, H. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted June 15, 2005 Accepted March 22, 2006 Relative efficacy of intravenous immunoglobulin G in ameliorating thrombocytopenia induced by anti-platelet GPIIbIIIa versus GPIb antibodies Michelle Lee Webster, Ebrahim Sayeh, Min Crow, Pingguo Chen, Bernhard Nieswandt, John Freedman, and Heyu Ni* The Canadian Blood Services, and St. Michael's Hospital, University of Toronto Institute of Clinical Biochemistry and Pathobiochemistry, and Rudolf Virchow Center for Experimental Toronto Platelet Immunobiology Group and Department of Laboratory Medicine, St. Michael's Hospital * Corresponding author; email: nih{at}smh.toronto.on.ca. Intravenous immunoglobulin G (IVIG) is used to treat idiopathic thrombocytopenic purpura (ITP). While many patients benefit from IVIG, some are refractory to this therapy. ITP is characterized by platelet clearance mediated primarily by anti-platelet antibodies against GPIIbIIIa and/or the GPIb complex. These two 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). Pre-treatment 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. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. Braun, J. E. Gessner, D. Varga-Szabo, S. N. Syed, S. Konrad, D. Stegner, T. Vogtle, R. E. Schmidt, and B. Nieswandt STIM1 is essential for Fc{gamma} receptor activation and autoimmune inflammation Blood, January 29, 2009; 113(5): 1097 - 1104. [Abstract] [Full Text] [PDF] 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 Haematologica, February 1, 2007; 92(2): 283 - 284. [Abstract] [Full Text] [PDF] D. S. Beardsley ITP in the 21st Century Hematology, January 1, 2006; 2006(1): 402 - 407. [Abstract] [Full Text] [PDF]

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