609 LOCALIZATION OF THE SITE OF ACTION OF A SERUM INHIBITOR OF ERYTHROPOIESIS

Serum IgG inhibitors of erythropoiesis have been found in adults with acquired pure red cell aplasia but have not been described in children. We studied the mechanism of action of such an inhibitor in a 51/2 year old male with acquired erythroblastopenia and severe anemia of 4 months duration. After an unsuccessful trial of corticosteroids, normal erythropoiesis was established with the administration of Cytoxan(CT). When the patient's erythroblastopenic marrow cells were cultured in plasma clots, increased numbers of CFU-E and BFU-E derived colonies formed in the presence of erythropoietin. Addition of the patient's pretreatment whole serum both to erythroblastopenic autologous marrow and to allogenic normal marrow cells suppressed CFU-E but not BFU-E derived colony formation. The specific inhibitor of CFU-E derived colony formation was present in the IgG fraction of the pretreatment serum. Whole serum obtained following the CT-induced remission no longer inhibited erythroid colony formation. Acquired pure red cell aplasia associated with a serum inhibitor occurs in the pediatric age group. Our findings suggest that this inhibitor is an IgG immunoglobulin which acts directly on the more mature CFU-E but not on the less differentiated BFU-E precursor.