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Blood, 14 May 2009, Vol. 113, No. 20, pp. 4963-4969. Prepublished online as a Blood First Edition Paper on January 14, 2009; DOI 10.1182/blood-2008-10-186064. This Article Full Text Full Text (PDF) Supplemental Tables All Versions of this Article: blood-2008-10-186064v1 113/20/4963    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Warkentin, T. E. Articles by Kelton, J. G. Search for Related Content PubMed PubMed Citation Articles by Warkentin, T. E. Articles by Kelton, J. G. Related Collections Immunobiology Thrombosis and Hemostasis Clinical Trials and Observations Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  THROMBOSIS AND HEMOSTASIS Studies of the immune response in heparin-induced thrombocytopenia Theodore E. Warkentin1,2, Jo-Ann I. Sheppard1, Jane C. Moore1,2, Richard J. Cook3, and John G. Kelton1,2 Departments of 1 Pathology and Molecular Medicine and 2 Medicine, Michael G. DeGroote School of Medicine, McMaster University, Hamilton, ON; and 3 Department of Statistics and Actuarial Science, University of Waterloo, Waterloo, ON Heparin-induced thrombocytopenia (HIT) is caused by platelet-activating antibodies that recognize PF4/heparin complexes. Uncertainties remain regarding HIT immunobiology, including the temporal relation of antibody formation to onset of thrombocytopenia, and whether immunoglobulin class switching occurs. Using serial plasma samples from 2 heparin thromboprophylaxis trials, we determined the time of onset, antibody levels, and immunoglobulin class distributions (IgG, IgA, IgM) for 12 patients with HIT and 36 patients who formed anti-PF4/heparin antibodies, but did not develop HIT ("seropositive non-HIT controls"). In patients with HIT, anti-PF4/heparin antibodies became detectable 4 days (median) after starting heparin; antibody detection preceded the platelet count decline by 2 days (median). Patients with HIT produced higher levels of IgG antibodies, but similar IgA and IgM levels, compared with seropositive non-HIT controls. Among all 48 seroconverting patients, the first day of a positive antibody test (median, day 6) did not differ among the immunoglobulin classes. Thus, the HIT immune response does not exhibit the classic paradigm of IgM class precedence/immunoglobulin class switching; rather, relatively rapid formation of IgG antibodies is observed, sometimes with concomitant IgA and IgM formation. Compared with seropositive non-HIT controls, HIT patients develop significantly higher anti-PF4/heparin IgG levels that are detectable before the onset of thrombocytopenia. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Nothing typical about HIT Gowthami M. Arepally Blood 2009 113: 4825-4826. [Full Text] [PDF] This article has been cited by other articles: G. M. Arepally Nothing typical about HIT Blood, May 14, 2009; 113(20): 4825 - 4826. [Full Text] [PDF]

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