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Prepublished online as a Blood First Edition Paper on July 12, 2002; DOI 10.1182/blood-2002-03-0765.
Submitted March 11, 2002
Accepted June 17, 2002
Rituximab in the treatment of acquired factor VIII inhibitors
Adrian Wiestner, Hearn J Cho, Adam S Asch, Mary Ann Michelis, Jack A Zeller, Ellinor I Peerschke, Babette B Weksler, and Geraldine P Schechter*
Hematology Branch, National Heart Lung and Blood Institute, Washington, D.C., USA
Weill Medical College, Cornell University, New York, N.Y., USA
Medical Center, Hackensack University, Hackensack, N.J., USA
Hematology Section, Veterans Affairs Medical Center, Washington, D.C., USA
* Corresponding author; email: G.P.Schechter{at}med.va.gov.
Autoantibodies against factor VIII (FVIII) are rare but can cause life-threatening bleeding requiring costly factor replacement and prolonged immunosuppression. We report four consecutively treated patients whose acquired FVIII inhibitors responded rapidly to immunosuppressive regimens that included rituximab, a monoclonal antibody against CD20+ B cells. Three patients had spontaneously occurring inhibitors. The fourth, a patient with mild hemophilia A, developed both an autoantibody and an alloantibody following recombinant FVIII treatment. Pretreatment FVIII activities ranged from <1% to 4% and inhibitor titers from 5 to 60 Bethesda units (BU). One patient with polymyalgia rheumatica who developed the inhibitor while receiving prednisone responded to single agent rituximab. The hemophilia patient had rapid resolution of the autoantibody whereas the alloantibody persisted for months. Responses continue off treatment from 7+ to 12+ months. This report adds to the growing evidence that rituximab has efficacy in immune disorders due to autoantibody formation.
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Acquired high-titer factor VIII inhibitor: fatal bleeding despite multimodal treatment including rituximab preceded by multiple plasmaphereses
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