Yatomi Y
Department of Laboratory Medicine, Yamanashi Medical University.
Nihon Rinsho. 1996 Sep;54(9):2397-401.
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.
本文描述了自身免疫性溶血性贫血的发病机制，包括温抗体型自身免疫性溶血性贫血（AIHA）、冷凝集素病（CAD）和阵发性冷血红蛋白尿（PCH）。这些溶血性贫血的特征是体内红细胞存活时间缩短，并有与自身红细胞反应的宿主抗体的证据。虽然红细胞自身抗体的病因仍有待解决，但已确定它们具有致病性。温反应性抗体通常促进脾脏和肝脏中的巨噬细胞对致敏红细胞的扣押，而冷反应性抗体则通过补体介导的机制导致致敏红细胞立即发生血管内溶血，或导致巨噬细胞对其扣押。
