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Epidemiology and pathophysiology of immune thrombocytopenic purpura


  • Conflicts of interest The author declares no conflicts of interest.

Terry Gernsheimer, MD, Associate Professor of Medicine, Division of Hematology, University of Washington School of Medicine, Puget Sound Blood Center, 21 Terry Avenue, Seattle, WA 98104, USA. Tel: (206) 292 6521; Fax: (206) 343 5043; e-mail:


Immune thrombocytopenic purpura (ITP) is characterized by the presence of antiplatelet antibodies and immune platelet destruction. The disorder has been described as having a predilection for young women over men. Bone marrow megakaryocytes appear morphologically and quantitatively normal, and early platelet kinetic studies were consistent with reduced platelet survival as the primary abnormality in ITP. During the last 10–20 yr, understanding of the kinetics of this disorder has evolved with evidence that platelet survival is not as abbreviated as previously thought. Thrombopoietin levels are only minimally elevated, if at all, suggesting marrow stimulation and platelet production may not be maximized. Megakaryocyte physiology appears to be altered in ITP, also suggestive of diminished platelet production. It appears both platelet survival and production are impaired in ITP. The epidemiology of ITP is reviewed here and the pathophysiology of ITP is reconsidered.