Journal
CURRENT OPINION IN HEMATOLOGY
Volume 25, Issue 5, Pages 373-381Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MOH.0000000000000447
Keywords
antibodies; desialylation; GPIb; GPIIbIIIa (IIb3 integrin); thrombocytopenia
Categories
Funding
- Canadian Institutes of Health Research [MOP 97918, MOP 119540, MOP 119551]
- Canadian Blood Services - Canadian Institutes of Health Research partnership fund [CIHR-BUC201403-HN-326400]
- Canadian Blood Services
- Canadian Institutes of Health Research Canadian Graduate Student - Master Award
- Laboratory Medicine and Pathobiology Departmental Fellowship from the University of Toronto
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Purpose of reviewImmune thrombocytopenia (ITP) is a common autoimmune bleeding disorder with as of yet, no established clinical prognostic or diagnostic biomarkers. Patients frequently experience a markedly decreased quality of life and may be at risk for severe/fatal haemorrhage. Here, we address discoveries in the pathogenesis of ITP, and novel therapeutic strategies in mouse models and human patients. Consolidation of these findings should be important in providing insight to establish future prognostic protocols as well as cutting-edge therapeutics to target refractory ITP.Recent findingsIt is unknown why a significant portion of ITP patients are refractory to standard treatments. Recent findings suggest distinct heterogeneity in ITP including antibody-mediated platelet activation, Fc-independent desialylated platelet clearance, attenuation of platelet-mediated hepatic thrombopoietin generation, and decreased CD8(+) T-suppressor generation. These mechanisms may partially explain clinical observations of increased refractoriness to standard therapies targeting classical Fc-dependent pathways. Moreover, these have initiated investigations into platelet desialylation as a diagnostic/prognostic marker and therapeutic target.SummaryRecent evidence of distinct ITP pathophysiology has opened new exploratory avenues for disease management. We will discuss the utility of investigations into these mechanisms of ITP and its potential impact in our understanding of pathogenesis and future treatment strategies.
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