Drug allergy

A drug allergy is an adverse reaction to a medication caused by the immune system. It differs from predictable side effects and nonimmune drug intolerance.

Drug hypersensitivity reaction: An unwanted reaction to a drug involving immune mechanisms or other forms of hypersensitivity. This broader category includes immune-mediated allergies and some reactions with similar symptoms.
Drug allergy testing: Clinical tests used to assess whether a person has an immune-mediated reaction to a medication. Testing can help distinguish true allergy from an inaccurate or outdated allergy label.
Adverse drug reaction: An unintended harmful response to a medication taken at normal doses. This umbrella includes drug allergies as well as predictable and nonimmune harms.
Anaphylaxis: A rapid, potentially life-threatening systemic hypersensitivity reaction affecting multiple organ systems. Some immediate drug allergies trigger this emergency, requiring prompt recognition and treatment.
Pharmacogenomics: The study of how genetic variation affects responses to medications. Genetic markers can identify elevated risk for certain drug hypersensitivity reactions.
Type I hypersensitivity: An immediate allergic reaction driven by IgE antibodies, mast cells, and released inflammatory mediators. This pathway accounts for many rapid reactions, including anaphylaxis after certain drugs.
Drug provocation test: A supervised procedure in which a patient receives a drug in increasing doses to assess tolerance or allergy. It can clarify uncertain histories when the expected benefit outweighs the risk.
Side effect: A secondary effect of a medication that can occur at usual therapeutic doses. Side effects such as nausea are not necessarily caused by an immune response.
Stevens–Johnson syndrome: A severe, usually drug-triggered mucocutaneous reaction involving epidermal injury and detachment. This rare delayed reaction makes identifying and permanently avoiding the culprit drug essential.
HLA-B*15:02: A human leukocyte antigen variant associated with increased risk of carbamazepine-induced Stevens–Johnson syndrome in some populations. Its association shows how inherited immune variation can guide drug-risk screening.

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