Garratty G
Am J Med Technol. 1976 Jun;42(6):209-19.
Ingestion of drugs can cause patients or blood donors to have a positive direct and sometimes indirect antiglobulin test. The most common cause of these positive reactions and immune hemolytic anemia due to drugs is the formation of red cell autoantibodies. These autoantibodies will react with the patient's own red cells and usually most other normal red cells in vitro without the drug being present. The prototype drug causing this type of reaction is alpha methyldopa (Aldomet). Other drugs cause positive antiglobulin tests by three different mechanisms, the drug antibodies reacting with red cells in vitro only in the presence of the drug. The first of these mechanisms causes positive reactions because the drug binds firmly to the red cell membrane, and antibody against the drug will combine with the drug on the membrane leading to IgG-sensitized red cells. The prototype drug for this mechanism is penicillin. The second mechanism involves chemical modification of the red cell membrane by the drug so that it takes up many proteins nonspecifically; the cephalosporins are the only group of drugs known to react in this fashion. The final mechanism involves the formation of an immune complex by the drug and its specific antibody. This immune complex will attach to cell membranes, usually activating complement in the process. Examples of drugs thought to operate by this mechanism are phenacetin, quinine, and quinidine. Some individuals have antibodies present in their serum that will react with chemical added to commercial blood bank reagents. Examples of these are antibodies to dyes added to ABO typing sera, antibodies to sodium caprylate in bovine albumin, and antibodies to chemicals added to red cell diluents, e.g., chloramphenicol, neomycin, and hydrocortisone. If these antibodies are present they can create problems in pretransfusion testing; in particular, they can present anomalies in ABO, Rh grouping, and antibody detection.
药物摄入可导致患者或献血者直接抗球蛋白试验呈阳性，有时间接抗球蛋白试验也呈阳性。药物导致这些阳性反应和免疫性溶血性贫血的最常见原因是红细胞自身抗体的形成。这些自身抗体将与患者自身的红细胞发生反应，并且在体外通常也会与大多数其他正常红细胞发生反应，此时药物并不存在。引发这类反应的典型药物是α-甲基多巴（爱道美）。其他药物通过三种不同机制导致抗球蛋白试验呈阳性，药物抗体仅在有该药物存在时在体外与红细胞发生反应。这些机制中的第一种导致阳性反应是因为药物牢固地结合在红细胞膜上，针对该药物的抗体将与膜上的药物结合，从而导致IgG致敏红细胞。这种机制的典型药物是青霉素。第二种机制涉及药物对红细胞膜的化学修饰，使其非特异性地摄取许多蛋白质；已知头孢菌素类药物是以这种方式发生反应的唯一一类药物。最后一种机制涉及药物与其特异性抗体形成免疫复合物。这种免疫复合物将附着在细胞膜上，通常在此过程中激活补体。据认为通过这种机制起作用的药物示例有非那西丁、奎宁和奎尼丁。一些人的血清中存在会与添加到商业血库试剂中的化学物质发生反应的抗体。其中包括针对添加到ABO血型分型血清中的染料的抗体、针对牛白蛋白中辛酸钠的抗体以及针对添加到红细胞稀释液中的化学物质（如氯霉素、新霉素和氢化可的松）的抗体。如果存在这些抗体，它们会在输血前检测中引发问题；特别是，它们会在ABO、Rh血型鉴定和抗体检测中呈现异常情况。
