Pathophysiology

Drug allergies are immune responses resulting from different mechanisms of immunologic recognition and activation, and reactions are produced by multiple physiologic pathways. This produces a confusing spectrum of clinical pictures and complex pathophysiologic mechanisms. Allergy is an adverse immune response to a stimulus and is traditionally placed in the Gell and Coombs categories: type I (immediate hypersensitivity), type II (complement-mediated antibody reactions), type III (immune complex reactions), and type IV (cellular or delayed-type hypersensitivity). Drug exposures often stimulate several or all of these types of reactions, and clinical symptoms do not always fit neatly into the categories.

The immune system uses many tools such as blood vessel dilation or constriction, causing fluid to flood an infected area, or even producing special cells to kill bacteria or the infected cells in which they harbor. The pattern of these responses is either inborn (the innate immune response) or learned from previous infections and injuries (the adaptive immune response). Most drug reactions involve the adaptive response and certainly, in the sense that they cause more harm than good, are "mistakes."

T cells control these "learned" responses and decide which "tools" to use in the reaction. Sometimes they choose several different "tools" at once, and multiple reactions ensue, as when a person becomes sensitized to penicillin and has not only anaphylaxis but hemolytic anemia and serum sickness, as well. There are different types of T cells, and they communicate either directly with other cells or by chemical messages, called "cytokines." The pattern of cytokines released is one way T cells have of determining which kind of response will occur. They are broadly called Th1 and Th2 responses, with Th1 mostly responding to infections and Th2 sometimes producing allergy or asthma.

Immunologic drug reactions generally represent T-cell activation. The type of T cell activated determines the type of reaction to the drug. Th1 cytokines (largely interferon^) produce many more chronic (and at times serious) skin reactions and destruction of cells (as in hemolytic anemia or thrombocytopenia). Sometimes these responses can damage tissues, such as the kidney (interstitial nephritis). Th2 cytokines tend to cause the antibodies produced to be switched to the immune globulin E (IgE) or allergic antibody class, which can result in hives or anaphylaxis. Other classes of antibodies are often made, and these can produce serum sickness or indirect destruction of cells (thrombocytopenia). T-cell receptors respond to one peptide only, which makes each activation response exclusive to the original stimulus (drug) or to chemical structures with very close resemblance.

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