Page 570 - Review of Medical Microbiology and Immunology ( PDFDrive )

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CHAPTER 65 Hypersensitivity (Allergy)
559
Receptor for
epsilon heavy chain
IgE
Allergen
Mast
Mast
cell
cell
cell

Mast cell with IgE bound Allergen cross-links IgE Mediators (e.g., histamine)
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released from mast cells
to surface; mediators
on mast cell surface
contained within granules
in cytoplasm
FIGURE 65–1
Immediate (anaphylactic) hypersensitivity.
gloves, which include urticaria, asthma, and even systemic
principal mediators in the bronchoconstriction of asthma
anaphylaxis. Table 65–3 summarizes some of the important
clinical aspects of immediate hypersensitivities.
and are not influenced by antihistamines.
(3) Eosinophil chemotactic factor of anaphylaxis
No single mediator accounts for all the manifestations of
type I hypersensitivity reactions. Some important media-
granules. When released during anaphylaxis, it attracts
tors and their effects are as follows:
eosinophils that are prominent in immediate allergic reac-
(1) Histamine occurs in granules of tissue mast cells (ECF-A) is a tetrapeptide that exists preformed in mast cell
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tions. The role of eosinophils in type I hypersensitivity
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and basophils in a preformed state. Its release causes
reactions is uncertain, but they do release histaminase and
vasodilation, increased capillary permeability, and
arylsulfatase, which degrade two important mediators, his-
smooth muscle contraction. Clinically, disorders such as
allergic rhinitis (hay fever), urticaria, and angioedema
reduce the severity of the type I response.
can occur. The bronchospasm so prominent in acute ana-
(4) Serotonin (hydroxytryptamine) is preformed in
phylaxis results, in part, from histamine release. Antihis-
mast cells and blood platelets. When released during ana-
tamine drugs block histamine receptor sites and can be
phylaxis, it causes capillary dilation, increased vascular
relatively effective in allergic rhinitis but not in asthma
permeability, and smooth muscle contraction but is of
(see later).
(2) Slow-reacting substance of anaphylaxis (SRS-A)
(5) Prostaglandins and thromboxanes are related to
consists of several leukotrienes, which do not exist in a
leukotrienes. They are derived from arachidonic acid via
preformed state but are produced during anaphylactic
the cyclooxygenase pathway. Prostaglandins cause dilation
reactions. This accounts for the slow onset of the effect of minor importance in human anaphylaxis.
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and increased permeability of capillaries and bronchocon-
SRS-A. Leukotrienes are formed from arachidonic acid by
striction. Thromboxanes aggregate platelets.
the lipoxygenase pathway and cause increased vascular
TABLE 65–3 Important Clinical Aspects of Immediate Hypersensitivities
Main Organ
Typical Allergens
Affected
Disease
Main Symptoms
Pollens, house dust (feces of dust
Wheezing, dyspnea, tachypnea
Inhalation
Asthma
Lung
mite), animal danders, many
occupational airborne allergens
Nose and eyes
Rhinitis, conjunctivitis,
“hay fever” Runny nose, redness and Pollens Contact with mucous
itching of eyes
membranes
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Skin
Uncertain
Uncertain
1. Eczema (atopic dermatitis)
Pruritic, vesicular lesions
1. Various foods
Ingestion

Pruritic, bullous lesions
2. Urticaria (hives)

Various

2. Drugs

Intestinal tract
Various foods
Allergic gastroenteropathy
Vomiting, diarrhea
Shock, hypotension, wheezing,
Sting
Anaphylaxis
1. Insect venom (e.g., bee venom)
Systemic

2. Drugs (e.g., penicillin)
pruritis, urticaria, asphyxia,

Various
cardiac arrest
Ingestion

3. Foods (e.g., peanuts)

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