Anaphylaxis is an acute, life-threatening, multisystem syndrome resulting from the sudden release of mediators by mast cells and basophils. Although
anaphylaxis is often under-communicated and thus underestimated, its incidence appears to have risen over recent decades. Drugs are among the most common triggers in adults, being
analgesics and
antibiotics the most common causal agents.
Anaphylaxis can be caused by immunologic or non-immunologic mechanisms. Immunologic
anaphylaxis can be mediated by
IgE-dependent or -independent pathways. The former involves activation of Th2 cells and the cross-linking of two or more specific
IgE (sIgE)
antibodies on the surface of mast cells or basophils. The
IgE-independent mechanism can be mediated by
IgG, involving the release of
platelet-activating factor, and/or complement activation. Non-immunological
anaphylaxis can occur through the direct stimulation of mast cell degranulation by some drugs, inducing histamine release and leading to anaphylactic symptoms. Work-up of a suspected
drug-induced
anaphylaxis should include clinical history; however, this can be unreliable, and skin tests should also be used if available and validated.
Drug provocation testing is not recommended due to the risk of inducing a harmful reaction. In vitro testing can help to confirm
anaphylaxis by analyzing the release of mediators such as
tryptase or
histamine by mast cells. When immunologic mechanisms are suspected, serum-sIgE quantification or the use of the basophil activation test can help confirm the culprit
drug. In this review, we will discuss multiple aspects of
drug-induced
anaphylaxis, including epidemiology, mechanisms, and diagnosis.