By far the largest proportion of side effects caused by non-steroidal anti-inflammatory drugs (NSAIDs) belong to the category of so-called PAR (pseudo-allergic reactions). The sensitising potential of a drug is probably connected with its protein-binding capacity. The strongly protein-binding compounds are particularly liable to produce serious immunological complications. The clinical picture depends on the type of immune reaction as well as its location within the organism. Cellular immunity usually leads to skin reactions. However, it is possible that some of the haematological side effects may be caused by T lymphocytes reacting specifically with haemopoietic cells to which a drug adheres. Antibody-mediated immune reactions are more common. Currently we can distinguish five different mechanisms. IgE-mediated drug reactions usually lead to eosinophilia, sometimes with eosinophilic infiltrates in the lung. In such cases, patients frequently develop urticarial rashes. In a number of drug-induced cytopenias the underlying mechanism derives from the action of soluble immune complexes on red cells, leucocytes or platelets as in the case of type I agranulocytosis. IgG and/or IgM may be implicated in the formation of the immune complexes. In this system, blood cells are affected when incubated with the serum from an allergic subject which has previously been incubated with the offending drug or one of its metabolites. Some drugs or drug metabolites have a strong affinity for certain blood cells to which they become attached. If a patient develops antibodies to these drugs, an antibody interaction with the drug-coated cells can lead to the destruction of the cells. This mechanism may be operative not only in the periphery, but also within the bone marrow. On serological testing, preincubation of the serum with the offending drug will inhibit the reaction of the antibody to drug-coated cells. This mechanism may coexist with the immune complex type of blood cell damage. It now appears that patients may develop antibodies whose specificity depends on a drug as well as on a component of the blood cell membrane. The haematological specificity of the immune reaction would then be explained by the autoantigenic constituent of the drug-autoantigen complex. This mechanism has been demonstrated with regard to blood group specificities of certain drug reactions in the case of red cells. In the case of quinidine and quinine thrombocytopenia, the antiplatelet activity has been shown to be connected with the presence of the glycoprotein GP1b which acts as a receptor for platelet factor VIII.(ABSTRACT TRUNCATED AT 400 WORDS)