Abdou N I, Verdirame J D, Amare M, Abdou N L
Ann Intern Med. 1981 Jul;95(1):43-50. doi: 10.7326/0003-4819-95-1-43.
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 less than 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 less than 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.
通过培养集落形成单位检测法（CFU-C）研究了21例再生障碍性贫血患者骨髓衰竭的机制。12例患者未检测到可导致CFU-C数量降低的体外缺陷。3例患者存在抑制CFU-C的抑制性T细胞（p<0.001）；2例患者中的1例对抗胸腺细胞球蛋白治疗有反应，第3例自发恢复。3例患者血清中存在针对其骨髓CFU-C的抑制性免疫球蛋白；血浆置换后骨髓功能恢复。3例患者在集落刺激因子水平存在异常：2例有集落刺激因子抑制剂，吲哚美辛和胆碱能激动剂可在体外和体内纠正（p<0.01）；第3例有集落刺激因子生成缺陷，锂可在体外和体内纠正。检测针对前体细胞的细胞或体液抑制因子或集落刺激因子水平的异常可为再生障碍性贫血的治疗提供有用的指导。
