Control of Antibody-Mediated Pure Red-Cell Aplasia by Plasmapheresis

Abstract

THE development of acquired pure red-cell aplasia in some patients is based on autoimmune mechanisms,^{1 , 2} as indicated by a favorable clinical response to immunosuppressive therapy^{3 4 5 6 7 8} and by the presence of IgG autoantibodies that impair various stages and mechanisms of erythropoiesis.^{9 10 11 12} The effects include interference with heme synthesis,⁹ as demonstrated in suspension cultures of normal bone marrow, complement-dependent lysis of erythroblasts,^{3 , 9} and complement-independent inhibition of erythroid burst and colony formation in culture by early erythroid progenitors.^{13 14 15 16} Occasionally, antibodies are directed against erythropoietin.^{17 , 18} This report describes a patient with pure red-cell aplasia whose plasma contained antibodies that inhibited erythroid burst formation of . . .