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Type Cause or Pathogenesis Histology * Clinical Features

Contact dermatitis Topically applied antigens Spongiotic dermatitis Marked itching, burning, or both; requires antecedent

exposure

Atopic dermatitis Unknown; may be heritable Spongiotic dermatitis Erythematous plaques in flexural areas; family history

of eczema, hay fever, or asthma

Drug-related eczematous dermatitis Systemically administered antigens or

haptens (e.g. penicillin)

Spongiotic dermatitis; infiltrate often

deeper with abundant eosinophils

Temporal relationship to drug administration; remits

with cessation of drug

Eczematous insect bite reaction Locally injected antigen or toxin Spongiotic dermatitis; wedge-shaped

infiltrate; many eosinophils

Papules, nodules, and plaques with vesicles; may be

linear when multiple

Photoeczematous eruption Ultraviolet light Spongiotic dermatitis; infiltrate that

diminishes gradually with depth

Occurs at sites of sun exposure; may require associated

exposure to systemic or topical antigen; photopatch

testing may help in diagnosis

Primary irritant dermatitis Repeated trauma or chemical irritants (as

in detergent)

Spongiotic dermatitis in early stages;

acanthosis predominates in later stages

Localized mechanical or chemical irritants

(nonimmunologic)

*All types, with time, may develop chronic changes, with prominent acanthosis of the epidermal layer.

The most obvious example is an acute contact reaction to topical antigens such as poison ivy, characterized by pruritic, edematous, oozing plaques, often containing small and large

blisters (vesicles and bullae) ( Fig. 25-25A ). Such lesions are prone to bacterial superinfection, which produces a yellow crust (impetiginization). With time, persistent lesions become

less "wet" (fail to ooze or form vesicles) and become progressively scaly (hyperkeratotic) as the epidermis thickens (acanthosis).

Pathogenesis.

This has been well studied in dermatitis due to contact hypersensitivity (e.g., poison ivy dermatitis). Initially, antigens at the epidermal surface are taken up by dendritic Langerhans

cells, which then migrate by way of dermal lymphatics to draining lymph nodes ( Fig. 25-26 ). Here, antigens, now processed by the Langerhans cell, are presented to naive CD4 T cells,

which are activated and develop into effector and memory cells ( Chapter 6 ). On antigen re-exposure,

Figure 25-25Eczematous dermatitis. A, In an acute allergic contact dermatitis, numerous vesicles appear at the site of antigen exposure (in this case, laundry detergent that persisted in

clothing). B, Histologically, intercellular edema produces widened intercellular spaces within the epidermis, eventually resulting in small, fluid-filled intraepidermal vesicles.

Figure 25-26Schematic diagram of mechanisms of allergic contact dermatitis. D, antigen; Ln, naive T lymphocyte; Lm, memory T lymphocyte.

Figure 25-27Erythema multiforme. A, The target-like clinical lesions consist of a central blister or zone of epidermal necrosis surrounded by macular erythema. B, Early lesions show



lymphocytes collecting along the dermal epidermal junction where basal keratinocytes have begun to become vacuolated.

Figure 25-28Clinical evolution of psoriasis. Early and eruptive lesions may be dominated by signs of inflammation and erythema (left). Established, chronic lesions demonstrate

erythema surmounted by characteristic silver-white scale (right). Rarely, the early inflammatory phase predominates throughout the course of the disease (pustular psoriasis).

Figure 25-29Psoriasis. Histologically, established lesions demonstrate marked epidermal hyperplasia, parakeratotic scale, and, importantly, minute microabscesses of neutrophils within

the superficial epidermal layers.

Figure 25-30Lichen planus. A, A solitary lesion of lichen planus (glistening surface is due to application of mineral oil, rendering the scale transparent). This flat-topped pink-purple,

polygonal papule shows prominent Wickham striae that are more easily appreciated through the transparent scale. B, Biopsy of one of the lesions demonstrates the bandlike infiltrate of

lymphocytes at the dermoepidermal junction and pointed rete ridges (saw-toothing; compare with Fig. 25-1 ).

Figure 25-31Lupus erythematosus. A, These chronic plaques show a thinned and glistening (atrophic) epidermis, areas where dilated and tortuous dermal vessels are apparent, and

central hypopigmentation surrounded by peripheral hyperpigmentation. Note areas of early hair loss due to follicular involvement. B, There is an infiltrate of lymphocytes within the

superficial and deep dermis, marked thinning of the epidermis with loss of normal rete ridges, and hyperkeratosis.

Figure 25-32Granular deposits of immunoglobulin (here IgG) and complement at the dermoepidermal junction constitute a positive "band test" in lupus erythematosus.

Figure 25-33Schematic representation of sites of blister formation. A, In a subcorneal blister, the stratum corneum forms the roof of the bulla (as in impetigo or pemphigus foliaceus). B,

In a suprabasal blister, a portion of the epidermis including the stratum corneum forms the roof (as in pemphigus vulgaris). C, In a subepidermal blister, the entire epidermis separates

from the dermis (as in bullous pemphigoid and dermatitis herpetiformis).

Figure 25-34Pemphigus vulgaris. A, Eroded plaques are formed on rupture of confluent, thin-roofed bullae, here affecting axillary skin. B, Suprabasal acantholysis results in an

intraepidermal blister in which rounded (acantholytic) epidermal cells are identified (inset).

Figure 25-35Direct immunofluorescence of pemphigus vulgaris. There is deposition of immunoglobulin along the plasma membranes of epidermal keratinocytes in a fishnet-like

pattern. Also note the early suprabasal separation due to loss of cell-to-cell adhesion (acantholysis).

Figure 25-36Bullous pemphigoid. Clinical bullae (A) result from basal cell layer vacuolization, producing a subepidermal blister (B). Histopathology of the edge of an early lesion

showing the onset of epidermal separation from the underlying dermis. Eosinophils, as well as lymphocytes and occasional neutrophils, may be intimately associated with basal cell layer

destruction, creating the subepidermal cleft.

Figure 25-37 A, Linear deposition of complement along the dermoepidermal junction in bullous pemphigoid; the pattern has been likened to ribbon candy. B, Bullous pemphigoid

antigen is located in the lowermost portion of the basal cell cytoplasm in association with hemidesmosomes (HD), with blister formation affecting the lamina lucida (LL) of the basement

membrane zone. LD, lamina densa; AF, anchoring fibrils.

Figure 25-38Dermatitis herpetiformis. A, Clinical lesions consist of intact and eroded erythematous blisters that are often grouped together. B, Histologically, neutrophilic

microabscesses selectively involve the dermal papilla.

Figure 25-39Dermatitis herpetiformis. A, Papillary dermal microabscesses are associated with zones of dermoepidermal cleavage that eventually coalesce to form a clinical blister. B,

By direct immunofluorescence, these abscesses are rich in IgA and fibrin deposits.

Figure 25-40Epidermolysis bullosa. A, Junctional epidermolysis bullosa showing typical erosions in flexural creases. B, A noninflammatory subepidermal blister in this case has formed

at the level of the lamina lucida (Giemsa-stained section).

Figure 25-41Porphyria. A noninflammatory blister is forming at the dermoepidermal junction; note the seemingly rigid dermal papillae at the base that contain the altered superficial

vessels.

Figure 25-42Acne. A, Inflammatory acne is characterized clinically by erythematous papules and pustules, with the possibility of eventual scarring. B, A portion of a hair shaft piercing

the follicular epithelium and eliciting an inflammatory response and fibrosis.

Figure 25-43Verruca vulgaris. A, Multiple papules with rough pebble-like surfaces. B (low power) and C (high power), histology of the lesions show papillomatous epidermal

hyperplasia and cytopathic alterations that include nuclear pallor and prominent keratohyaline granules. D, In situ hybridization showing viral DNA within epidermal cells.

Figure 25-44Molluscum contagiosum. A focus of verrucous epidermal hyperplasia contains numerous cells with ellipsoid cytoplasmic inclusions (molluscum bodies) within the stratum

granulosum and stratum corneum.

Figure 25-45Tinea. A, Characteristic plaque of tinea corporis. Routine histology (B) shows the picture of mild eczematous (spongiotic) dermatitis, and periodic acid-Schiff stain reveals

deep red hyphae and yeast forms (C) within the stratum corneum.

Figure 25-46 A, Pediculosis. Egg case (nit) of head louse attached to hair shaft. B, Portions of a scabies mite within a burrow involving the stratum corneum.

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