[Pathogenesis of erythrocyte destruction in autoimmune hemolytic anemia]

Abstract

The pathogenesis of autoimmune hemolytic anemias, including warm type autoimmune hemolytic anemia (AIHA), cold agglutinin disease (CAD), and paroxysmal cold hemoglobinuria (PCH), is described. These hemolytic anemias are characterized by shortening of erythrocyte survival in vivo and evidence of host antibodies reactive with autologous erythrocytes. Although the etiology of erythrocyte autoantibodies remains to be solved, it is established that they are pathogenic. Warm-reactive antibody usually facilitates the sequestration of sensitized erythrocytes by macrophages in spleen and liver, whereas cold-reactive antibodies cause either immediate intravascular hemolysis of sensitized erythrocytes by complement-mediated mechanism or their sequestration by macrophages.