Serological Methods for the Detection of Drug-induced Allergic Blood

Drugs can produce blood disorders in many ways. At one end of the spectrum are dose-dependent effects which can be explained in pharmacological terms as 'toxic' reactions. At the other end of the spectrum are dose-independent effects which cannot be predicted. With the discovery of the causal relationship between amidopyrine intake and agranulocytosis in certain patients, increasing attention has been paid to the latter phenomena and a number of distinct immune mechanisms have been elucidated in drug-induced blood dyscrasias. The first mechanism is similar to that encountered in experimental serum sickness (Cochrane and Koffler, 1973). The thrombocytopenia and leucopenia in this condition is probably due to the effect of immune complexes on the cells: platelets and leucocytes, coated with antigen-antibody complexes, are eliminated from the circulating blood, presumably through phagocytosis by the reticuloendothelial system (Miescher, 1955; Mannick Haakenstad, and Arend, 1974). A similar immunecomplex type mechanism is likely to be operative in many cases of drug-induced thrombocytopenia and leucopenia. The second mechanism has been used for many years as a serological tool for the detection of antibodies and is the agglutination of antigen-coated red cells by antibody (passive hemagglutination). Damage to drug-coated cells by drug-specific antibodies is today a well recognized mechanism in certain drug-induced cytopenias. A third mechanism emerged from the clinical observation that certain drugs lead to the development of autoantibodies, ie, antibodies directed to autologous antigenic determinants. In this review, these three mechanisms are discussed first and serological methods available for diagnosis of immune drug-induced blood dyscrasias will be discussed later.