Type I IgE antibody-mediated reactions

Type I, IgE Antibody-Mediated Reactions to Sulfonamide Antimicrobials... 

For many years, two terms, anaphylaxis and anaphylactoid, have been used to describe relatively rare reactions that have features commonly associated with severe immediate, often life-threatening, allergic reactions. These two terms are distinguished by the underlying mechanisms of the reactions. The term anaphylaxis is used by many for an immune IgE antibody-mediated, systemic immediate type I hypersensitivity reaction, often occurring within seconds or minutes. 

Type I reactions are IgE antibody-mediated. Receptor-bound drug-reactive IgE on the surface of mast cells is cross-linked by complementary drug determinants causing cell degranulation and the release of inflammatory mediators. 

Penicillins can cause all four types of hypersensitivity responses provoking type I IgE-mediated reactions such as urticaria, angioedema, asthma, and anaphylaxis type n antibody-mediated hemolytic anemia and thrombocytopenia type III immune complex-mediated serum sickness-like reactions and vasculitis and type IV T cell-mediated contact dermatitis, rashes, and other skin eruptions (refer to Chaps. 2 and 3). Table 5.1 lists clinical adverse reactions, together with their immune... 

The range and diversity of adverse effects provoked by contrast media remain poorly understood and hence difficult to categorize. For the allergist and clinical immunologist used to thinking of immediate reactions as type I allergic responses mediated by IgE antibodies and delayed reactions as type IV hypersensitivity reactions mediated by antigen-specific effector T cells, adverse reactions to contrast media, divided... 

Type I allergic reactions are inappropriate immune responses to an allergen with preferential synthesis of immunoglobulin E (IgE), a special antibody class, which binds to mast cells and basophilic granulocytes via Fee receptors. Binding of the allergen to the cell-bound IgE initiates the rapid release of allergic mediators, most prominently histamine, and the de novo synthesis of arachidonic acid metabolites and cytokines, which are responsible for the clinical symptoms. 

Type I reactions occur when the drug or its bound hapten incites an IgE antibody response. IgE binds to high-affinity receptors on mast cells and basophils. When the original antigen cross-links the cell-bound IgE, the effector cell releases enormous amounts of preformed mediators, producing the... 

Most anaphylactoid reactions are due to a direct or chemical release of histamine, and other mediators, from mast cells and basophils. Immune-mediated hypersensitivity reactions have been classified as types I-IV. Type I, involving IgE or IgG antibodies, is the main mechanism involved in most anaphylactic or immediate hypersensitivity reactions to anaesthetic drugs. Type II, also known as antibody-dependent hypersensitivity or cytotoxic reactions are, for example, responsible for ABO-incompatible blood transfusion reactions. Type III, immune complex reactions, include classic serum sickness. Type IV, cellular responses mediated by sensitised lymphocytes, may account for as much as 80% of allergic reactions to local anaesthetic. 

The patient experienced an anaphylactic response to the penicillin. This is a type I (immediate) drug reaction, mediated by IgE antibodies. The answer is (D). 

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