The effect of rituximab on anti‐platelet autoantibody levels in patients with immune thrombocytopenia. (25th April 2017)

• Record Type: Journal Article
• Authors: Arnold, Donald M.; Vrbensky, John R.; Karim, Nadia; Smith, James W.; Liu, Yang; Ivetic, Nikola; Kelton, John G.; Nazy, Ishac
• Is Part Of: British journal of haematology. Volume 178:Number 2(2017)
• Page Start: 302
• Page End: 307
• Publication Date: 2017-04-25
• Subjects: immune thrombocytopenia -- rituximab -- autoantibody -- anti‐GPIIbIIIa -- anti‐GPIbIX; Hematology -- Periodicals; Blood -- Diseases -- Periodicals; 616.15
• DOI: 10.1111/bjh.14664
• Languages: English
• ISSNs: 0007-1048

Abstract

Summary: Rituximab is an effective therapy resulting in a platelet count improvement in 60% of patients with immune thrombocytopenia (ITP). Rituximab depletes B cells; thus, a reduction in platelet autoantibody levels would be anticipated in patients who achieve a clinical response to this treatment. The objectives of this study were to determine whether rituximab was associated with a reduction in platelet autoantibody levels, and to correlate the loss of autoantibodies with the achievement of a treatment response. We performed a case‐control study nested within a previous randomized controlled trial of standard therapy plus adjuvant rituximab or placebo. We measured platelet‐bound anti‐glycoprotein (GP) IIbIIIa and anti‐GPIbIX using the antigen capture test. Of 55 evaluable patients, 25 (45%) had a detectable platelet autoantibody at baseline. Rituximab was associated with a significant reduction in anti‐GPIIbIIIa levels ( P = 0·02) but not anti‐GPIbIX levels ( P = 0·51) compared with placebo. Neither the presence of an autoantibody at baseline nor the loss of the autoantibody after treatment was associated with a response to rituximab. The subset of patients with persistent autoantibodies after treatment failed to achieve a platelet count response, suggesting that persistence of platelet autoantibodies can be a marker of disease severity.