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 Blood, 25 June 2009, Vol. 113, No. 26, pp. 6511-6521.
Prepublished online as a Blood First Edition Paper on April 24, 2009; DOI 10.1182/blood-2009-01-129155.

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REVIEW ARTICLE

The ITP syndrome: pathogenic and clinical diversity

Douglas B. Cines1,2, James B. Bussel3, Howard A. Liebman4, and Eline T. Luning Prak1

Departments of 1 Pathology and Laboratory Medicine and 2 Medicine, University of Pennsylvania, Philadelphia; 3 Departments of Pediatrics, Obstetrics-Gynecology, and Medicine, Weill Medical Center College of Cornell University, New York, NY; and 4 Department of Medicine, University of Southern California, Los Angeles

Immune thrombocytopenia (ITP) is mediated by platelet autoantibodies that accelerate platelet destruction and inhibit their production. Most cases are considered idiopathic, whereas others are secondary to coexisting conditions. Insights from secondary forms suggest that the proclivity to develop platelet-reactive antibodies arises through diverse mechanisms. Variability in natural history and response to therapy suggests that primary ITP is also heterogeneous. Certain cases may be secondary to persistent, sometimes inapparent, infections, accompanied by coexisting antibodies that influence outcome. Alternatively, underlying immune deficiencies may emerge. In addition, environmental and genetic factors may impact platelet turnover, propensity to bleed, and response to ITP-directed therapy. We review the pathophysiology of several common secondary forms of ITP. We suggest that primary ITP is also best thought of as an autoimmune syndrome. Better understanding of pathogenesis and tolerance checkpoint defects leading to autoantibody formation may facilitate patient-specific approaches to diagnosis and management.


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F. Rodeghiero, M. Ruggeri, and on behalf of the International Working Group
Response:Immune thrombocytopenic purpura: terminology and definitions
Blood, August 27, 2009; 114(9): 2004 - 2004.
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