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20-52: Allergic & Immunologic Disorders

Teresa K. Tarrant; Mildred Kwan

Allergy is an immune-mediated hypersensitivity reaction to a foreign antigen manifest by tissue inflammation and organ dysfunction. The clinical expression of allergic IgE-mediated disease depends on antigen exposure and host susceptibility manifesting as atopy. Atopic patients have an immunologic predisposition to several disorders: allergic rhinitis (see Chapter 8), allergic asthma (see Chapter 9), atopic dermatitis (see Chapter 6), and IgE-mediated food allergies. Although these disorders tend to aggregate in atopic families, each of these disorders may occur in individuals without personal or familial history of atopic disease. In addition, many mast cell– and IgE-dependent disorders (eg, many drug and chemical sensitivities, eosinophilic disorders, mast cell stability syndromes, chronic urticaria) occur with a similar incidence in atopic and non-atopic persons.

The timing of onset of allergic symptoms after exposure to a suspected allergen serves as a useful clinical marker on which to base diagnosis and treatment. Reactions are either immediate (occurring within 60–120 minutes after initial exposure) or delayed (occurring after several hours or up to several weeks after initial exposure) (eTable 20–3).

eTable 20–3.Classification of immunologically mediated hypersensitivity reactions.
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eTable 20–3. Classification of immunologically mediated hypersensitivity reactions.
Classification Effector Mechanism Timing of Reaction Clinical Manifestations Associated Conditions
Type I (Immediate, IgE-mediated)

Crosslinking of IgE bound to FcεRs on mast cells causing degranulation and release of inflammatory mediators, eg, histamine, tryptase.

 Within 60–120 minutes

Anaphylaxis (see Table 20–13 for NIAID/FAAN criteria)

 

Rhinorrhea, sneezing, watery/itchy eyes

Wheezing, shortness of breath

Food allergy

Drug allergy

Venom allergy

Allergic rhinitis

Asthma
Type II (IgG- or IgM-mediated)

Direct IgG/IgM binding to antigen/hapten on cell surface leading to complement activation and cell destruction.

 Hours to days

Hemolytic anemia, thrombocytopenia, neutropenia

 Drug-induced, immune-mediated anemia, thrombocytopenia, neutropenia
Type III (Immune complex)

Deposition of antibody-antigen immune complexes in tissue capillary beds resulting in complement activation, leukocyte recruitment and inflammation.

1–3 weeks following antigen exposure

 Fever, arthralgia, rash, lymphadenopathy, glomerulonephritis, vasculitis

Serum sickness associated with drugs and venom

Drug-induced vasculitis
Type IV (Delayed, cell- mediated)

Antigen-mediated T-cell activation leading to recruitment of leukocytes, release of inflammatory mediators including cytokines and cell cytotoxicity/cell death.

Typically 48–72 hours following antigen exposure

Rash (typically maculopapular), bullous exanthema, hepatitis

Allergic contact dermatitis

Delayed-type drug rash

SCARs

SJS/TEN

DRESS

AGEP

 

 

AGEP, acute granulomatous exanthematous pustulosis; DRESS, drug reaction with eosinophilia and systemic symptoms; FAAN, Food Allergies and Anaphylaxis Network; NIAID, National Institute of Allergies and Infectious Diseases; SCARs, severe cutaneous adverse reactions; SJS, Stevens-Johnson syndrome; TEN, toxic epidermal necrolysis.

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