835a - 836: A Study of the Mechanisms of Formation of Para-Erythroblasts

In hemolytic anemia, and above all during the perinatal age, the blood and bone marrow display an increased erythroblastic proliferation which Schridde (1910) considers as a reactional phenomenon and Rautmann (1912) as a nosologic entity: erytroblastic disease. The pathological morphology of the nuclei of the normoblasts was illustrated by Introzzi (1926), Diamond (1932), Blackfan and Baty (1932). Lehndorff (1934) considers it due to a mutation.Critical study of the literature and the experiments performed by the author have led to the following conclusions:1.In normally maturing erythroblasts, with dense and sometimes pyknotic nucleus, this is rounded and expelled “in toto” without appreciable deformation and with no fragmentation.2.The normoblasts with twin nuclei observed in various pathological states, especially during hemolytic anemia of the perinatal age, are pathological forms.3.At the present stage of our knowledge, Lehndorff’s hypothesis is not acceptable regarding a special erythroblastic line — para-erythroblasts — produced by mutation of the genes controlling the morphology of blood cells.4.It appears more likely that the nuclear deformation is produced as the consequence of an antigen-antibody humoral conflict. The immunizing proteins: maternal antibodies anti-Rh or auto-antibodies, penetrate the normoblasts and, there, come into contact with the respective specific antigens.A consequence of the immunizing conflict is that partial reduction of the surface tension occurs in the nucleo-cytoplasmic interphase which leads to the formation of “shoots” and the transformation of the normoblastic nucleus into the pathological form of paraerythroblasts.