Drug side effects are a significant public health problem in modern medicine. Drug hypersensitivity reactions are a relativly common side effect that is categorized as a type B side effect. The mechanisms underlying drug hypersensitivity reactions are most often explaind using the concept of allergic-immune stimulation by haptens, which is based on the general classification of hypersensitivity reactions published in 1963 by the authors Gell and Coombs. This classification of hypersensitivity reactions is divided into four types depending on the underlying immune mechanism. Type 1 reactions are mediated by immunoglobulin E and leed to the development of a classical clinical picture of an allergic reaction. Type 2 reactions are mediated by immunoglobulins M or G directed against cell components or the extracellular matrix. Type 3 reactions are mediated by immunocomplexes which by precipitating into tissues result in an inflammatory reaction. Type 4 reactions are mediated by cellular immunity. Although the occurrence of most drug hypersensitivity reactions can be explained by the concept of hypersensitivity according to Gell and Coombs, the concept of pharmacological drug interactions with immunoreceptors (p-i concept) has recently been proposed to supplement our knowledge of hypersensitivity reactions and their pharmacogenetic basis. According to the p-i concept, drugs can bind directly to immune receptors and directly activate the cellular immune response whicih results in the occurence of drug hypersensitivity reactions. The clinical picture of drug hypersensitivity reactions is diverse, ranging from benign skin rashes to life-threatening conditions such as anaphylaxis or toxic epidermal necrolysis. The diagnostic procedure in case of suspicion of a drug hypersensitivity reaction is based on an extensive history, skin and laboratory testing, and provocation testing.