Hypersensitivity reactions represent exaggerated or inappropriate immune responses that can result in significant tissue injury and systemic manifestations. Among the four classical types described in the Gell and Coombs classification, Type I hypersensitivity—also known as immediate hypersensitivity—is mediated predominantly by immunoglobulin E (IgE) and is responsible for a wide spectrum of allergic disorders, ranging from mild atopic reactions to severe, life-threatening anaphylaxis. This review focuses on the immunological basis, etiology, epidemiology, and pathophysiology of Type I hypersensitivity reactions. Sensitization to environmental, food, or drug antigens leads to IgE production and its binding to high-affinity Fcε receptors on mast cells and basophils. Subsequent re-exposure to the antigen triggers rapid mast cell degranulation and the release of preformed mediators, lipid-derived mediators, cytokines, and chemokines, resulting in acute and late-phase allergic inflammation. Key mechanistic concepts, including the hapten hypothesis, pro-hapten hypothesis, and pharmacological interaction (p-i) concept, are discussed to explain drug-induced immediate hypersensitivity. The review also highlights epidemiological trends, common triggers such as foods and medications, and emerging evidence of alternative IgG-mediated pathways in anaphylaxis. A comprehensive understanding of these mechanisms is essential for accurate diagnosis, effective management, and prevention of immediate hypersensitivity reactions and their long-term complications.
Sayed* et al. (Sat,) studied this question.