Miura A
3rd Department of Internal Medicine, Akita University School of Medicine.
Nihon Rinsho. 1996 Sep;54(9):2534-8.
Acquired drug-related hemolytic anemia is mainly induced by immune mechanism or microvascular lesion. Three mechanisms of drug-related immunologic injury to red blood cells are recognized. They are hapten or drug adsorption mechanism, ternary or drug-antibody-target cell complex mechanism and autoantibody mechanism. Prototype drugs are penicillin, quinidine and alpha-methyldopa, respectively. Symptoms are mild to moderate in cases of hapten and autoantibody mechanisms and ameliorate by withdrawal of the drugs. Hemolytic anemia due to ternary mechanism may have severe even fetal symptoms, including hemoglobinemia and hemoglobinuria. Some antineoplastic agents can cause hemolytic anemia that resembles the hemolytic uremic syndrome. The prototype drug is mitomycin.
获得性药物相关性溶血性贫血主要由免疫机制或微血管病变引起。目前已认识到药物对红细胞产生免疫损伤的三种机制。它们分别是半抗原或药物吸附机制、三元或药物 - 抗体 - 靶细胞复合物机制和自身抗体机制。原型药物分别是青霉素、奎尼丁和α-甲基多巴。半抗原和自身抗体机制引起的症状较轻至中度,停药后症状改善。三元机制导致的溶血性贫血可能有严重甚至危及胎儿的症状,包括血红蛋白血症和血红蛋白尿。一些抗肿瘤药物可引起类似于溶血尿毒综合征的溶血性贫血。原型药物是丝裂霉素。