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Restored platelet function after romiplostim treatment in a patient with immune thrombocytopenic purpura

Gardiner, E.E., Thom, J.Y., Al-Tamimi, M., Hughes, A., Berndt, M.C., Andrews, R.K. and Baker, R.I. (2010) Restored platelet function after romiplostim treatment in a patient with immune thrombocytopenic purpura. British Journal of Haematology, 149 (4). pp. 625-628.

Link to Published Version: http://dx.doi.org/10.1111/j.1365-2141.2010.08092.x
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Abstract

Whilst the precipitating aetiology of immune thrombocytopenic purpura (ITP) remains unclear, the predominant cause of the thrombocytopenia is the presence of circulating antiplatelet autoantibodies that coat platelets, leading to platelet destruction and clearance, primarily in the spleen. Traditional clinical management of patients with ITP, including treatment with corticosteroids, intravenous immunoglobulins, splenectomy, rituximab, and cyclophosphamide, aims to curb platelet destruction (Nurden et al, 2009a). Newer reagents approved for trial to treat ITP patients, such as thrombopoietin mimetics, romiplostim (Kuter et al, 2008) and eltrombopag, act primarily in the bone marrow to stimulate thrombopoiesis. Whilst neither plasma thrombopoietin levels nor platelet production kinetics are markedly altered in ITP patients, ITP anti-platelet autoantibodies interfere with megakaryocyte proliferation and platelet production in vitro (Chang et al, 2003). Here we describe a significant improvement to the nature and function of platelet immunoreceptor tyrosinebased activation motif (ITAM) receptors in an ITP patient with an autoantibody to platelet glycoprotein (GP)VI receiving romiplostim.

Publication Type: Journal Article
Murdoch Affiliation: Centre for Haemophilia and Thrombosis Research
Publisher: Blackwell Publishing Inc.
Copyright: Blackwell Publishing Ltd.
Notes: Correspondence
URI: http://researchrepository.murdoch.edu.au/id/eprint/3718
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