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002). TPO levels may have diagnostic utility in discriminating between patients with hypoproliferative and consumptive thrombocytopenia. Elevated TPO levels in ITP patients may predict a poor clinical response to treatment with TPO receptor agonists. Am. J. Heamtol. 88:1041�C1044, 2013. ? 2013 Wiley Periodicals, Inc. Thrombopoietin (TPO) is the major regulator of platelet production. Prior studies in animal models [1-3] http://www.selleckchem.com/products/epz-5676.html and humans [4] have demonstrated that TPO levels vary inversely with circulating platelet mass. Additional clinical studies have suggested that TPO levels also vary inversely with the rate of megakaryopoiesis [5-10]. Thus, TPO levels may help distinguish between the various disorders of thrombocytopenia, with elevated TPO levels associated with hypoproliferative thrombocytopenia (e.g., aplastic anemia) but normal TPO levels associated with consumptive thrombocytopenia (e.g., immune thrombocytopenia) [5-8, 10]. In addition, the introduction of TPO receptor agonists for the treatment of thrombocytopenia has created an interest in predicting the response of patients to these agents [11]; TPO levels may help predict treatment http://www.selleckchem.com/products/ly2109761.html responses. To assess the performance characteristics of a TPO assay in a clinical setting, we measured the serum TPO concentration in a panel of healthy humans as well as patients with diverse hematologic diseases. We then correlated the TPO level with platelet count, diagnosis, and treatment response. Our goals were (1) to determine the normal range of TPO levels, (2) to determine http://www.selleck.cn/products/Staurosporine.html whether TPO levels could help discriminate between different disorders of platelet production, and (3) determine whether TPO levels might help predict the platelet response in those patients treated with a TPO receptor agonist (either eltrombopag or romiplostim). Between March 2010 and May 2011, serum samples were collected from patients with diverse hematologic diseases affecting the platelet count who verbally consented to participate in the study. Samples were allowed to clot and the serum separated by centrifugation (1,500g for 15 min). Serum aliquots were stored at ?80��C until testing. At the time of sample collection, relevant demographic and clinical data such as the diagnosis, platelet count, and prior clinical and medication history were recorded for each patient from the electronic medical record. Clinical diagnoses were made according to standard criteria [12-14]. The study was approved by the Massachusetts General Hospital Institutional Review Board. Serum TPO concentration was measured using a quantitative sandwich ELISA (R&D Systems, Minneapolis, MN) [9, 10]. Briefly, 0.2 mL of serum was incubated in wells coated with a mouse monoclonal antibody specific for human TPO. After washing, captured TPO was detected using a polyclonal horseradish peroxidase-conjugated goat anti-TPO antibody. TPO was quantified using a standard curve created with glycosylated recombinant human TPO provided in the ELISA kit.