Page 866 - Robbins Basic Pathology by Vinay Kumar, Abul K. Abbas, Jon C. Aster
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852 C H A P T E R 23 Skin activation of complement (Chapter 3). The ensuing urticaria
affects the lips, throat, eyelids, genitals, and distal extremities.
bulla. Blister is common term for both vesicles and When the larynx is affected, the condition can be dangerous,
bullae. since airway patency may be compromised.
Microscopic Terms MORPHOLOGY
Acantholysis: Loss of intercellular adhesion of
keratinocytes. The histologic features of urticaria often are subtle. There is
Acanthosis: Diffuse epidermal hyperplasia. usually a sparse superficial perivenular infiltrate of mononu-
Dyskeratosis: Abnormal keratinization occurring pre- clear cells, rare neutrophils, and sometimes eosinophils.
maturely within individual cells or groups of cells below Superficial dermal edema creates more widely spaced colla-
the stratum granulosum. gen bundles. Degranulation of mast cells, which normally
Hyperkeratosis: Hyperplasia of the stratum corneum, reside around superficial dermal venules, is difficult to appre-
often associated with a qualitative abnormality of ciate with routine hematoxylin-eosin (H&E) stains but can be
keratin. highlighted using a Giemsa stain.
Lentiginous: Linear melanocyte proliferation along the
epidermal basal cell layer; can occur as a reactive change Clinical Features
or as part of a melanocytic neoplasm. Urticaria typically affects persons between 20 and 40 years
Papillomatosis: Surface elevation caused by hyperplasia of age, but no age is immune. Individual lesions usually
and enlargement of dermal papillae. develop and fade within hours, but episodes can persist for
Parakeratosis: Keratinization characterized by retention days or even months. Persistent lesions sometimes are due
of the nuclei in the stratum corneum. On squamous to urticarial vasculitis, which is often associated with depo-
mucosal membranes, such as buccal mucosa, parakera- sition of complement in dermal venules. Lesions range in
tosis is normal. size and nature from small, pruritic papules to large, edem-
Spongiosis: Intercellular edema of the epidermis. atous, erythematous plaques. Increased vascular permea-
bility leads to localized dermal edema. Lesions can be
ACUTE INFLAMMATORY confined to a particular part of the body or generalized. In
DERMATOSES a specific type of urticaria, termed pressure urticaria, lesions
are found only in areas exposed to pressure (such as the
Thousands of inflammatory dermatoses exist, challenging feet or the buttocks). Although not life-threatening, urti-
the diagnostic acumen of even experienced clinicians. In caria can compromise quality of life by causing severe pru-
general, acute lesions last from days to weeks and are char- ritus and social embarrassment. Most cases are treated with
acterized by inflammation (often marked by mononuclear antihistamines. Systemic steroids are used in more severe
cells rather than neutrophils and defined as acute due to refractory cases.
the limited course of their natural history), edema, and
sometimes epidermal, vascular, or subcutaneous injury. Acute Eczematous Dermatitis
Some acute lesions may persist, resulting in transition
to a chronic phase, while others are characteristically Eczema is a clinical term that embraces a number of condi-
self-limited. tions with varied underlying etiologies. New lesions take
the form of red papules, often with overlying vesicles, which
Urticaria ooze and become crusted. With persistence, these lesions
develop into raised, scaling plaques. The nature and degree
Urticaria (“hives”) is a common disorder mediated by of these changes vary among the clinical subtypes, which
localized mast cell degranulation, which leads to dermal micro- include the following:
vascular hyperpermeability. The resulting erythematous, • Allergic contact dermatitis, which stems from topical
edematous, and pruritic plaques are termed wheals.
exposure to an allergen
PAT H O G E N E S I S • Atopic dermatitis, which has traditionally been attributed
In most cases, urticaria stems from an immediate (type 1) to allergen exposure, but is now thought to stem from
hypersensitivity reaction (Chapter 4), in which antigens defects in keratinocyte barrier function, many with a
trigger mast cell degranulation by binding to immunoglobulin genetic basis
E (IgE) antibodies displayed on the mast cell surface. The • Drug-related eczematous dermatitis, a hypersensitivity
responsible antigens include pollens, foods, drugs, and insect reaction to a drug
venom. IgE-independent urticaria may result from exposure • Photoeczematous dermatitis, in which eczema appears as
to substances that directly incite mast cell degranulation, such an abnormal reaction to UV or visible light
as opiates and certain antibiotics. In the vast majority of • Primary irritant dermatitis, which results from exposure
cases, no clinical cause is discovered despite extensive search- to substances that chemically, physically, or mechani-
ing. Hereditary angioedema is caused by an inherited defi- cally damage the skin
ciency of C1 esterase inhibitor, which results in uncontrolled In most cases, the skin lesions resolve completely when the
offending stimulus is removed or exposure is limited,
