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Chronic Idiopathic Thrombocytopenic Purpura: Mechanisms of Pathogenesis

¹University of Washington Medical School–Seattle, Puget Sound Blood Center, Seattle, Washington, USA

Key Words. Thrombocytopenia • Platelets • ITP • Thrombopoietin

Correspondence: Correspondence: Terry Gernsheimer, M.D., 921 Terry Avenue, Seattle, Washington 98104-1256, USA. Telephone: 206-292-6521; Fax: 206-343-5043; e-mail: bldbuddy{at}u.washington.edu

Received June 13, 2008; accepted for publication November 25, 2008.

Disclosure: Employment/leadership position: None; Intellectual property rights/inventor/patent holder: None; Consultant/advisory role: Terry Gernsheimer, Amgen, GlaxoSmithKline, MGI Pharma; Honoraria: Terry Gernsheimer, Amgen, GlaxoSmithKline; Research funding/contracted research: Terry Gernsheimer, Amgen, GlaxoSmithKline, and MGI Pharma; Ownership interest: None; Expert testimony: None; Other: None. The content of this article has been reviewed by independent peer reviewers to ensure that it is balanced, objective, and free from commercial bias. No financial relationships relevant to the content of this article have been disclosed by the authors, planners, independent peer reviewers, or staff managers.

The mechanism of idiopathic (autoimmune) thrombocytopenic purpura (ITP) has historically been attributed to platelet autoantibody production and the resultant platelet destruction. More recent evidence suggests a multifactorial pathogenesis. A complex picture of the immune processes involved in autoimmunity has emerged over the last decade with the identification and characterization of immunoregulatory elements (receptors, cytokines, and other signaling molecules) and cell trafficking patterns. An understanding of the interplay of cellular and humoral immune responses in the breakdown of self-tolerance has brought to light unrecognized mechanisms of the autoimmune destruction of platelets in ITP and potential targets for future therapeutic advances. The failure of the bone marrow to maximally increase platelet production also appears to play an important role in the thrombocytopenia of ITP. Treatment strategies targeting the thrombopoietin receptor to increase platelet production are a promising new approach to the management of ITP.