The understanding of ITP pathophysiology has strengthened over the decades:

• 1950s: Drs. William Harrington and James Hollingswood demonstrated that ITP is caused by a plasma factor and is therefore a disease of platelet destruction.^1,2
  
• 1960s: Splenic removal of platelets, rather than intravascular destruction, was found to be a major mechanism of platelet loss.³
  
• 1970s: Several studies reported elevated platelet-associated immunoglobulin G (PAIgG). This test was found to be too nonspecific to be clinically useful, but it confirmed the utility of antibody detection and measurement. ⁴
  
• 1980s: In the 1980s the conventional wisdom held that the known increase in platelet destruction in ITP had an associated increase in platelet production. However, platelet survival studies done to test the concept showed that platelets production in most ITP patients was decreased, or at best, in the normal range. ^5,6
  
• 21st century: Many avenues of investigation continue to increase our understanding of ITP:
  
  • More about thrombopoietin (TPO): Research suggests that decreased or ineffective platelet production is an important aspect of ITP, as seen by the role of TPO in the regulation of the production process.^7,8
    
  • Role of megakaryocytes: Antiplatelet autoantibodies not only destroy platelets but also lead to suppression of marrow megakaryocytes and thus impair thrombopoiesis in ITP.^7,8
    
  • Platelet antigen mimicry: Although the factors that initiate autoantibody production are unknown, evidence suggests that the antigens responsible for initiating the autoimmune response are altered platelet proteins or viral or bacterial products that mimic platelet antigens.⁹

Read more about the Regulation of Platelet Production.

References

1. Bromberg ME. Immune thrombocytopenic purpura—the changing therapeutic landscape. New Engl J Med. 2006;355(16):1643-1645.
2. McMillan R, Nugent D. The effect of antiplatelet autoantibodies on megakaryocytopoiesis. Intern J Hematol. 2005;81(2):94-99.
3. Shulman NR, Marder VJ, Weinrach RS. Similarities between known antiplatelet antibodies and the factor responsible for thrombocytopenia in idiopathic purpura. Physiologic, serologic and isotopic studies. Ann NY Acad Sci 1965;124(2):499-542.
4. Cines DB, McMillan R. Pathogenesis of chronic immune thrombocytopenic purpura. Curr Opin Hematol. 2007;14:511-514.
5. Ballem PJ, Segal GM, Stratton JR, Gernsheimer T, Adamson JW, Slichter SJ. Mechanisms of thrombocytopenia in chronic autoimmune thrombocytopenic purpura. Evidence of both impaired platelet production and increased platelet clearance. J Clin Invest. 1987;80(1):33-40.
6. Heyns Adu P, Badenhorst PN, Lotter MG, Pieters H, Wessels P, Kotze HF. Platelet turnover and kinetics in immune thrombocytopenic purpura: results with autologous ¹¹¹In-labeled platelets and homologous ⁵¹Cr-labeled platelets differ. Blood. 1986;67(1):86-92.
7. Chang M, Nakagawa PA, Williams SA, et al. Immune thrombocytopenic purpura (ITP) plasma and purified ITP monoclonal autoantibodies inhibit megakaryocytopoiesis in vitro. Blood. 2003;102(3):887-895.
8. McMillan R, Wang L, Tomer A, Nichol J, Pistillo J. Suppression of in vitro megakaryocyte production by antiplatelet autoantibodies from adult patients with chronic ITP. Blood. 2004;103(4):1364-1369.
9. Chong BH, Ho S-J. Autoimmune thrombocytopenia. J Thromb Haemost. 2005;3(8):1763-1772.