ITP is perhaps best seen as a disorder of both increased platelet destruction and suboptimal platelet production.1 The TPO pathway plays a central role in platelet production and—in ITP—this pathway is disrupted.2 Addressing the functional deficiency of TPO in ITP patients may lead to a better understanding of the management of this disease.
Since antiplatelet antibodies were first identified, ITP therapy has focused primarily on inhibiting platelet destruction. Most current medical treatments either disrupt the function of macrophages in the reticuloendothelial system or inhibit the production of antiplatelet antibodies. This approach has been effective for many patients; however, some patients relapse, and others do not initially respond to medical therapy. Splenectomy is often used after failing other treatments.3
Read more about treatment for ITP.
References
1. Chong BH, Ho S-J. Autoimmune thrombocytopenia. J Thromb Haemost. 2005;3(8):1763-1772.
2. Emmons RVB, Reid DM, Cohen RL, et al. Human thrombopoietin levels are high when thrombocytopenia is due to megakaryocyte deficiency and low when due to increased platelet destruction. Blood. 1996;87(10):4068-4071.
3. Bromberg ME. Immune thrombocytopenic purpura—the changing therapeutic landscape. New Engl J Med. 2006;355(16):1643-1645.
