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Immediate Hypersensitivity Reactions

Background

The immune system is an integral part of human protection against disease. The normally protective immune mechanisms can sometimes cause detrimental effects in the host called hypersensitivity reactions. A hypersensitivity reaction is an inappropriate or exaggerated response to an antigen or an allergen. The traditional classification for hypersensitivity reactions is that of Gell and Coombs and is currently the most commonly known classification system.
It divides the hypersensitivity reactions into the following 4 types:

Type I reactions (i.e., immediate hypersensitivity reactions) involve immunoglobulin E (IgE)–mediated release of histamine and other mediators from mast cells and basophils.
Examples include anaphylaxis and allergic rhinoconjunctivitis.

Type II reactions (i.e., cytotoxic hypersensitivity reactions) involve immunoglobulin G or immunoglobulin M antibodies bound to cell surface antigens, with subsequent complement fixation. An example is drug-induced hemolytic anemia.

Type III reactions (i.e., immune-complex reactions) involve circulating antigen-antibody immune complexes that deposit in postcapillary venules, with subsequent complement fixation. An example is serum sickness.

Type IV reactions (i.e., delayed hypersensitivity reactions, cell-mediated immunity) are mediated by T cells rather than by antibodies. An example is contact dermatitis from poison ivy or nickel allergy.

Some authors believe this classification system may be too general and favor a more recent classification system proposed by Sell et al.
This system divides immunopathologic responses into the following 7 categories:

Inactivation/activation antibody reactions

Cytotoxic or cytolytic antibody reactions

Immune-complex reactions

Allergic reactions

T-cell cytotoxic reactions

Delayed hypersensitivity reactions

Granulomatous reactions

This system accounts for the fact that multiple components of the immune system can be involved in various types of hypersensitivity reactions. For example, T cells play an important role in the pathophysiology of allergic reactions (see Pathophysiology). In addition, the term immediate hypersensitivity is somewhat of a misnomer because it does not account for the late-phase reaction or for the chronic allergic inflammation that often occurs with these types of reactions.

Allergic reactions manifest clinically as anaphylaxis, allergic asthma, urticaria, angioedema, allergic rhinoconjunctivitis, some types of drug reactions, and atopic dermatitis. These reactions tend to be mediated by IgE, which differentiates them from non-IgE-mediated (formerly called anaphylactoid) reactions that involve IgE-independent mast cell and basophil degranulation. Such reactions can be caused by iodinated radiocontrast media (RCM), opiates, or vancomycin and appear similar clinically to urticaria or even anaphylaxis.

Patients prone to IgE-mediated allergic reactions are said to be atopic. Atopy is the genetic predisposition to make IgE antibodies in response to allergen exposure.

The focus of this article is allergic reactions in general. Although some of the clinical manifestations listed previously are briefly mentioned, refer to the articles on these topics for more detail. For example, see Allergic and Environmental Asthma; Anaphylaxis; Food Allergies; Rhinitis, Allergic; and Urticaria.

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