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Effect of Interleukin-3 on Responsiveness to Granulocyte-Colony-stimulating Factor in Severe Aplastic Anemia

Klaus Geissler, MD; Christa Forstinger, MD; Peter Kalhs, MD; Paul Knöbl, MD; Peter Kier, MD; Paul Kyrle, MD; and Klaus Lechner, MD
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Requests for Reprints: Klaus Geissler, MD, First Clinic of Internal Medicine, University of Vienna, Währingergürtel 18-20, A-1090 Vienna, Austria.

Current Author Addresses: Drs. Geissler, Forstinger, Kalhs, Knöbl, Kier, Kyrle, and Lechner: First Clinic of Internal Medicine, University of Vienna, Währingergürtel 18-20, A-1090 Vienna, Austria.

Ann Intern Med. 1992;117(3):223-225. doi:10.7326/0003-4819-117-3-223
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Some patients with aplastic anemia show temporary improvements in hematopoiesis after monotherapy with hematopoietic growth factors (1-3), but those with severe cases rarely respond (4). Inadequate response in these patients is thought to be caused by a profound deficiency of hematopoietic progenitors (5). We recently reported that interleukin-3 effectively expands the pool of hematopoietic progenitors in primates, suggesting that this molecule may be used therapeutically to make hematopoiesis more responsive to late-acting cytokines (6). Pretreatment with interleukin-3 has been shown to potentiate the effects of granulocyte-macrophage colony-stimulating factor on myelopoiesis (7), of erythropoietin on erythropoiesis (8), and of interleukin-6 on


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