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

  
@article{AOB4700,
	author = {Jan Zlamal and Tamam Bakchoul},
	title = {Acquired immune thrombocytopenia: an update on pathophysiology, diagnosis and management},
	journal = {Annals of Blood},
	volume = {3},
	number = {0},
	year = {2018},
	keywords = {},
	abstract = {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 (},
	issn = {2521-361X},	url = {https://aob.amegroups.org/article/view/4700}
}