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Treatment of acquired factor VIII deficiency with rituximab

Treatment of acquired factor VIII deficiency with rituximab

Blood 96(11 Part 2): 84b, November 16

In April 1997, a 75-year-old African-American male presented with a spontaneous soft tissue hemorrhage into his neck. Tracheostomy was required to protect the airway. He was diagnosed with an acquired deficiency in factor VIII (factor VIII activity level less than 1%, factor VIII inhibitor level 150 Bethesda units). He was successfully treated with a combination of porcine factor VIII, human factor VIII and recombinant human factor VIIa (rFVIIa). He continued to suffer spontaneous hemarthrosis and soft tissue hemorrhages. Attempts to treat his underlying condition with prednisone; cyclophosphamide vincristine and prednisone; dexamethasone and cyclosporin; and intravenous immune globulin were all unsuccessful. His hemorrhages were managed with FEIBA until rFVIIa became commercially available. In March 2000, the patient was receiving rFVIIa on a daily basis for treatment of hemorrhage into his thighs. A decision was made to treat him with rituximab. The factor VIII inhibitor level of the patient was measured at 525 Bethesda units, with factor VIII activity level of less than 1% prior to institution of rituximab therapy. On April 4, 2000, the first of four weekly doses of rituximab, dosed at 375 mg/m2/week was administered without toxicity. There was a clinical response to therapy as the patient has suffered only one spontaneous hemorrhage since the administration of rituximab. There was a laboratory response to therapy as the factor inhibitor level was measured at 315 Bethesda units four weeks after completion of the rituximab therapy. Sixteen weeks after completion of the therapy, the factor VIII inhibitor level was measured at 67 Bethesda units with a factor VIII level of 7%. This case suggests that rituximab may have a role in the treatment of patients with acquired inhibitors to factor VIII.

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