New understanding of drug hypersensitivity mechanism
In the last few years, we came to a better understanding of the underlying immunological mechanisms of drug hypersensitivity reactions (DHRs). Therefore, DHRs have been classified into allergic, pharmacological interaction (p-i concept) and pseudoallergic. In allergic reaction the drug act as hapten and specific immune response is directed against a hapten-carrier complex (the hapten hypothesis). This can be mediated by IgE and IgG antibodies or by T cells. According to the type of reactions these reactions can be immediate or nonimmediate. Elicitors are: beta-lactactams- BLs, sulphanilamides, quinolones, metamizol, radiocontrast media- RCM, neuromuscular blocking agent- NMBA and antineoplastics. In p-i concept the drug can bind directly to HLA or TCR. p-i reactions are considered nonimmediate. The most frequent elicitors are: BLs, sulphanilamides, quinolones, metamizol, RCM, vancomycin, antineoplastics, anticonvulsants, local anaesthetics and abacavir. In pseudoallergic reaction the drug binds directly to the receptor or interact with enzymes of effector cells. These reactions are considered immediate. Type of drugs eliciting DHRs by pseudoallergic mechanism are: nonsteroidal anti-inflammatory drugs- NSAIDs, quinolones, RCM, NMBA and vancomycin.1,2