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Heterogeneity of Pathogenetic Mechanisms in Aplastic Anemia: Efficacy of Therapy Based on In-Vitro Results

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Grant support: the Veterans Administration; grant AI-15360, National Institutes of Health; Mid-America Cancer Center Program; the Kansas Chapter of the Arthritis Foundation; and the Kansas City Chapter of the Lupus Foundation.

Presented November 1980, at the Central Society for Clinical Investigation Meeting, Chicago, Illinois.

▸Requests for reprints should be addressed to Nabih I. Abdou, M.D., Ph.D.; Division of Allergy, Clinical Immunology, and Rheumatology, Room 416C, University of Kansas Medical Center, Kansas City, KS 66103.

Kansas City, Kansas; and Kansas City, Missouri

© 1981 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1981;95(1):43-50. doi:10.7326/0003-4819-95-1-43
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The mechanisms responsible for the bone marrow failure in 21 aplastic anemia patients were studied by the colony-forming units in culture assay (CFU-C). Twelve patients had no detectable in-vitro defect that could be responsible for the low CFU-C numbers. Three patients had suppressor T cells that inhibited CFU-C (p < 0.001); one of two patients responded to antithymocyte globulin therapy and the third recovered spontaneously. Three patients had serum inhibitory immunoglobulins directed against their marrow CFU-C; plasmapheresis resulted in recovery of bone marrow function. Three patients had abnormalities at the colony-stimulating factor level: Two had inhibitors of colony-stimulating factor, corrected in vitro and in vivo by indomethacin and cholinergic agonists (p < 0.01); and the third had colony-stimulating factor generation defect, corrected in vitro and in vivo by lithium. Testing for cellular or humoral suppressor factors directed against precursor cells or for abnormalities at the colony-stimulating factor level gives helpful guidelines to therapy in aplastic anemia.





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