Thromb Haemost 2002; 88(06): 892-897
DOI: 10.1055/s-0037-1613330
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Schattauer GmbH

Acute Thrombocytopenia in Patients Treated with the Oral Glycoprotein IIb/IIIa Inhibitors Xemilofiban and Orbofiban: Evidence for an Immune Etiology

Authors

  • Jacqueline A. Brassard

    3   Pharmacia Corporation, St. Louis MO
  • Brian R. Curtis

    1   The Blood Research Institute, Blood Center of Wisconsin, Milwaukee, WI
  • Richard A. Cooper

    2   Medical College of Wisconsin, Milwaukee, WI
  • John Ferguson

    3   Pharmacia Corporation, St. Louis MO
  • Wendy Komocsar

    3   Pharmacia Corporation, St. Louis MO
  • Maria Ehardt

    1   The Blood Research Institute, Blood Center of Wisconsin, Milwaukee, WI
  • Stuart Kupfer

    3   Pharmacia Corporation, St. Louis MO
  • Clement Maurath

    3   Pharmacia Corporation, St. Louis MO
  • Edward Swabb

    3   Pharmacia Corporation, St. Louis MO
  • Christopher P. Cannon

    4   The Brigham and Women’s Hospital, Boston Massachusetts, U.S.A.
  • Richard H. Aster

    1   The Blood Research Institute, Blood Center of Wisconsin, Milwaukee, WI
    2   Medical College of Wisconsin, Milwaukee, WI

Supported by grants HL-13629 and HL-44612 from the National Heart, Lung, and Blood Institute.
Further Information

Publication History

Received 20 May 2002

Accepted after resubmission 13 August 2002

Publication Date:
09 December 2017 (online)

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Summary

Thrombocytopenic episodes occurring in 18,845 patients treated with the GPIIb/IIIa inhibitors xemilofiban and orbofiban (“fibans”) were analyzed by a blinded review panel and 73 patients were classified as having “possible fiban-induced thrombocytopenia”. When the treatment codes were broken, a significant association between drug exposure and assignment to this group was found (p <0.001). Twenty-eight (82%) of 34 archived serum samples from these patients contained fiban-dependent antibodies specific for GPIIb/IIIa, but no such antibodies were found in 61 drug treated patients not classified as having “possible fiban-induced thrombocytopenia” (p <0.001). We conclude that fiban-dependent antibodies were the major cause of acute, severe thrombocytopenia in patients judged on the basis of clinical findings to have thrombocytopenia “possibly-induced” by xemilofiban and orbofiban. Measurement of drug-dependent antibodies may be helpful in determining the basis for acute thrombocytopenia in fiban-treated patients and possibly for identification of patients at risk to develop thrombocytopenia.