Acquired immune thrombocytopenia: an update on pathophysiology, diagnosis and management

Jan Zlamal, Tamam Bakchoul


Acquired thrombocytopenias represent a group of bleeding diseases which can be mediated by immune or non-immune factors. Acquired immune thrombocytopenia (AITP) leads to an accelerated decrease in platelet count by platelet reactive antibodies arising from several mechanisms. In AITP, autoantibodies (AAbs), alloantibodies or drug-dependent antibodies (DDAbs) are usually targeting platelet surface glycoproteins (GPs). The consequence of this is a significant decrease in the number of circulating platelets, leading to clinicopathological disorders including immune thrombocytopenia (ITP), heparin-induced thrombocytopenia (HIT) or drug-induced thrombocytopenia (DITP), respectively. The aforementioned disorders are characterized by a severe reduction in platelet count (<20×109/L) which is, with the exception of HIT, associated with high bleeding risk. In this review we provide current insight into recent achievements regarding pathophysiology, diagnosis and management of AITP.