Article

Rituximab in the treatment of acquired hemophilia

Department of Pharmacy Practice, College of Pharmacy, University of Illinois Medical Center at Chicago, 60612-7229, USA.
Annals of Pharmacotherapy (Impact Factor: 2.92). 07/2006; 40(6):1151-7. DOI: 10.1345/aph.1G658
Source: PubMed

ABSTRACT To review published literature evaluating the use of rituximab for treatment of acquired hemophilia.
An English-language literature search was conducted using MEDLINE (1966-January 2006). References of identified articles were subsequently reviewed for additional data. Search terms included rituximab, acquired hemophilia, and inhibitors.
Available data suggest that B-cell depletion by rituximab in patients with acquired hemophilia may contribute to the eradication of inhibitors to coagulation factors. B-cells have been shown to be essential in the development of autoimmunity or an acquired immune response. Beneficial effects of rituximab, after failure of established therapies, have been reported in case reports and one small, open-label trial.
Although data are limited, administration of rituximab appears to be an effective option for treatment of patients with acquired hemophilia after established therapies have failed. Patients given rituximab experienced cessation of recurrent bleeding, normalization of factor VIII activity, and eradication of inhibitors. A complete response to rituximab (undetectable inhibitors, normalization of factor levels) generally occurred several weeks to months after initiation of therapy.

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    • "As compared with acquired haemophilia, which is always due to auto-antibodies against FVIII, the pathogenic mechanisms underlying AVWS are more heterogeneous. Previous reports have shown that rituximab is an option for the correction of acquired haemophilia (Stachnik, 2006). For our two patients with AVWS, rituximab was initiated 1 month after the last administration of IVIg, as an alternative treatment, expecting a correction of their disease and the FVIII/VWF complex. "
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    ABSTRACT: Hemophilia A is classically caused by a congenital deficiency of factor VIII, but an acquired form due to inhibitors to factor VIII (FVIII) typically presents later in life. Patients who develop such acquired factor VIII inhibitors may present with catastrophic bleeding episodes, despite having no prior history of a bleeding disorder. Though the disorder is rare, it is known to cause significant morbidity and mortality. This review will focus on what is currently known about acquired hemophilia A, its pathogenesis, its associated etiologies, and its treatment.
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    ABSTRACT: Currently, the only proven strategy for achieving antigen-specific tolerance to factor VIII (FVIII) is immune tolerance induction (ITI) therapy. This paper discusses our current knowledge of the host and treatment factors, as well as supportive care initiatives, known or suspected to influence the outcome of ITI in the treatment of inhibitors arising in patients with severe hemophilia A. Among these, questions surrounding the choice of therapeutic product and/or dosing regimen generate the most controversy, given the lack of a definitive evidence-based approach to either. Furthermore, the potential for central venous access device (CVAD) and intercurrent bleeding complications to impact the ultimate success of ITI remains unclear. The ongoing clinical trials designed to further clarify several of these polarizing issues are reviewed. This paper also explores the current and future role of immune modulation in possible salvage, ancillary or primary alternative tolerance induction strategies. The special cases of low titer/ responding inhibitors and inhibitors developing in mild hemophilia A patients are considered. Finally, this paper summarizes the currently recommended approach to ITI and makes the case for a move from empiric therapeutics to a risk-stratified evidence-based approach to FVIII inhibitor eradication.
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Joan Stachnik