Abstract
Aplastic anemia (AA) is a disorder characterized by bone marrow failure leading to pancytopenia. The underlying cause remains unknown in most cases. Several mechanisms have been implicated in the pathogenesis of the disease, including an intrinsic stem cell defect, lymphocyte-mediated suppression of hemotopoiesis, dysfunction of the bone marrow microenvironment, and abnormalities in regulation of hematopoiesis by humoral factors (Nissen-Druey 1989). Elevated levels of interferon-γ in the serum (Zoumbos et al. 1985) and increased production of tumor necrosis factor-α by mononuclear cells (Hinterberger et al. 1988), both potent inhibitors of hematopoiesis, have been described in A A. Monocyte interleukin-1 (IL-1) production is decreased in A A patients (Nakao et al. 1988). However, elevated levels of serum burst-promoting activity (BPA) and colony-stimulating activity (CSA) have been reported (Adams and Barrett 1985; Nissen et al. 1985; Yen et al. 1985). In previous studies, we demonstrated that elevated CSA is attributable mainly to granulocyte-macrophage colony-stimulating factor (GM-CSF) in the serum (Schrezenmeier et al. 1989). Elevated levels of BPA, CSA and GM-CSF are correlated with severity and prognosis of the disease (Nissen et al. 1985; Schrezenmeier et al. 1989).
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Schrezenmeier, H., Noé, G., Rich, I.N., Raghavachar, A. (1992). Serum Erythropoietin Levels in Aplastic Anemia Determined by ELISA. In: Pagel, H., Weiss, C., Jelkmann, W. (eds) Pathophysiology and Pharmacology of Erythropoietin. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-77074-6_27
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DOI: https://doi.org/10.1007/978-3-642-77074-6_27
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