BASIC SCIENCE Mechanisms of platelet recovery in ITP associated with therapy Sophie J. Y. Pang & Alan H. Lazarus Received: 31 August 2009 / Accepted: 29 January 2010 / Published online: 24 February 2010 # Springer-Verlag 2010 Abstract Immune thrombocytopenia (ITP) is an autoim- mune disease primarily characterized by increased clearance of auto-antibody-sensitized platelets by Fc-receptor-bearing macrophages in the spleen and liver. It has been classically accepted that antibody-mediated platelet destruction is Fc dependent. Recent studies, however, may also indicate the involvement of Fc-independent pathways of platelet destruc- tion. Current treatment options work by immunosuppression (e.g., corticosteroids), immunomodulation (e.g., IVIg and anti-D), or removal of the platelet destruction site (splenecto- my) in ITP. This review will discuss the mechanisms of action of these and other treatments for ITP. Keywords ITP . Therapy . IVIg . Anti-D . Corticosteroids . Splenectomy . Helicobacter pylori Introduction Immune thrombocytopenia (ITP) is an autoimmune disease generally characterized by increased clearance of auto- antibody-sensitized platelets by Fc-receptor (FcR)-bearing macrophages [1, 2]. In addition, decreased platelet produc- tion is partly responsible for the reduced platelet count in ITP [3]. The disorder varies in its severity and clinical presentation. The terminology used to describe ITP and its treatment outcomes has been recently revised and standard- ized and an international consensus on the investigation and management of ITP has also recently been published [4, 5]. Recently diagnosed childhood ITP is often preceded by viral infection. Most childhood cases resolve spontaneous- ly, regardless of whether treatment is given. Up to 20% become chronic with the ITP persisting for more than 12 months. In contrast to childhood ITP, ITP in adults typically occurs with an unknown cause and is not generally associated with an underlying disorder [1]. It is currently accepted that antibody-mediated platelet destruction is Fc dependent. Recent studies however, may also indicate the involvement of Fc-independent pathways of platelet destruction [6–10]. Current treatment options work by immunosuppression (e.g., corticosteroids), immu- nomodulation (e.g., IVIg and anti-D), or removal of the platelet destruction site (splenectomy). The heterogeneity of ITP etiology makes the disorder unpredictable in its requirement for, and response to, therapy. Mechanisms of platelet destruction in ITP In order to understand platelet recovery with treatment, the causes of ITP need to be defined. A review of the literature S. J. Y. Pang : A. H. Lazarus (*) The Canadian Blood Services, Toronto, ON, Canada e-mail: lazarusa@smh.toronto.on.ca S. J. Y. Pang : A. H. Lazarus The Keenan Research Centre, Li Ka Shing Knowledge Institute of St Michael’ s Hospital, Toronto, ON, Canada S. J. Y. Pang : A. H. Lazarus The Toronto Platelet Immunobiology Group and The Departments of Medicine, Laboratory Medicine & Pathobiology of the University of Toronto, Toronto, ON, Canada A. H. Lazarus St. Michael’ s Hospital, 30 Bond Street, Toronto, ON, Canada M5B 1W8 Ann Hematol (2010) 89 (Suppl 1):S31–S35 DOI 10.1007/s00277-010-0916-2