At the center of the field are giant proerythroblast with intensely basophilic cytoplasm, a loose nuclear chromatin structure, and very large nucleoli. This cell is several times larger than a normal erythroblast and is roughly the size of a megakaryocyte.
This severe reduction of erythropoiesis in the bone marrow occurs mainly in children but may also develop in hemolytic anemias aplastic crisis.
Parvovirus B19 infection has been identified as the causal agent for the decreased erythropoiesis and consequent reticulocytopenia.
The diagnosis is established by the presence of giant proerythroblasts in the bone marrow, which reach the size of megakaryocytes. Most cases resolve spontaneously in 1 to 2 weeks.
This phenomenon involves a syncytium-like aggregation of erythroblasts, which form pale cytoplasmic bridges at points of atypical papillary urothelial hyperplasia between the individual cells. On electron microscopy it is characterized by the presence of septate-like membrane junctions between erythroblasts which are caused by a monoclonal immunoglobulin which is directed against an antigen of erythroblast membrane resulting in isolated severe anaemia with reticulocyto The Anemia in this case responded after therapy with corticosteroids.
The diagnosis may be suggested by characteristic morphological appearance of bone parazitii 20 cm smears, and further atypical papillary urothelial hyperplasia by electron microscopy. Ultrastructural examination of abnormal erythroblast clusters show that these cells were closely approximated with characteristic intercellular membrane junctions.
Moreover, synartesis of normal erythroblasts were induced by the patient IgG fraction. Immunogold labeling showed that the monoclonal IgG were detected in, and restricted to, the synartesis.
A discrete monoclonal plasmacytosis was also found in the patient bone marrow. The adhesion receptor CD36 appeared to be concentrated in the junctions, suggesting that it might be involved in atypical papillary urothelial hyperplasia synartesis.
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These experiments indicated that a monoclonal serum immunoglobulin IgG in the present cases directed at erythroblast membrane antigen was responsible for the erythroblast abnormalities. Specific therapy of the underlying lymphoproliferation was followed by complete remission of the anemia in these cases.