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- W2045152334 abstract "Abstract. Modern concepts of haematopoiesis and its regulation are reviewed. Observations from several forms of aplastic anaemia are analysed in the light of this new knowledge. The pathogenetic mechanism in the aplasia caused by chloramphenicol is probably a stem cell damage of an autoimmune or idiosyncratic nature. Chlorpromazine aplasia is apparently due to a constitutionally defective DNA synthesis, so that a normal compensatory reaction cannot take place against the inhibiting effects of the drug on DNA synthesis. The chlorpromazine aplasia is normally transient, since transit cells of the bone marrow—and not the stem cells—are affected. The hepatitis‐associated aplasia may possibly be precipitated by an autoimmune attack on multipotent stem cells or on transit cells of one or more cell lines after virus‐induced change of antigenicity of the cell surface. The thymoma‐associated aplasia may likewise be due to autoimmunity directed against transit cells. Finally, there are indications that the Fanconi aplasia may be pathogenetically heterogeneous, with constitutionally defective stem cells, transit cells, or stromal cells. Otherwise stromal failure rarely seems to play a role in human aplastic anaemia. Furthermore, “maturation arrest” probably does not exist. Neither “stem cell exhaustion” nor situations with missing or defective haemopoietins apparently produce aplasia on their own. A research strategy, supplementary to the routine haematological investigations, is proposed. It is recommended that modern immunological techniques in particular should be applied in combination with stem cell assays." @default.
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- W2045152334 date "1974-01-12" @default.
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- W2045152334 title "APLASTIC ANAEMIA: CONSIDERATIONS ON THE PATHOGENESIS" @default.
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- W2045152334 doi "https://doi.org/10.1111/j.0954-6820.1974.tb01006.x" @default.
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