Granulocyte Mediator Release in Pseudo-allergic Reactions

Abstract

Acetylsalicylic acid (ASA) and other nonsteroidal anti-inflammatory drugs are among the most frequent causes of adverse drug reactions. The clinical symptoms often resemble allergy and consist of anaphylactic shock, bronchospasm, urticaria, and angioedema [8]. However, there is no evidence, that immune mechanisms, which are specific for the eliciting agent, are involved and therefore it has been suggested that such reactions should be designated as “pseudo-allergic reactions” (PAR) [9]. Besides their nonspecifity, PAR are distinguished from allergic reactions, by the fact that they occur at the first administration and thus do not need a sensitization phase, they are not transferable to other individuals of the same species, and they are not acquired but rather constitute a heriditary trait. There is evidence that the similarity of PAR and allergic reactions results from the fact that similar mediators and amplification systems are involved, for example, nonspecific release of histamine from mast cells or basophils [3] or activation of other granulocyte subsets; activation of thrombocytes [1]; activation of complement [7, 10]; or drug-induced influence on mononuclear cells resulting in altered release of cytokines. However, the pathogenesis of PAR remains unknown. Since skin tests are not reliable, the diagnosis relies on history and risky provocation tests. Therefore, the purpose of this study was to screen different leukocyte functions in order to establish in vitro test systems, thereby increasing our knowledge about the pathogenesis of PAR.