Page 867 - Robbins Basic Pathology by Vinay Kumar, Abul K. Abbas, Jon C. Aster

Acute Inflammatory Dermatoses 853

stressing the importance of investigating the underlying
cause. Only the most common form, contact dermatitis, is
considered here.

Contact dermatitis is triggered by exposure to an envi-
ronmental contact sensitizing agent, such as poison ivy,
that chemically reacts with self-proteins. The self-proteins
modified by the agent are processed by epidermal Langer-
hans cells, which migrate to draining lymph nodes and
present the antigen to naive T cells. This sensitization event
leads to acquisition of immunologic memory; on reexpo-
sure to the antigen, the activated memory CD4+ T lympho-
cytes migrate to the affected skin sites. There they release
cytokines that recruit additional inflammatory cells and
also mediate epidermal damage, as in any delayed-type
hypersensitivity reaction (Chapter 4).

MORPHOLOGY A

In the case of contact dermatitis, the pattern of skin involve- B
ment is limited to sites of contact with the triggering agent
(Fig. 23–1, A), whereas in other forms of eczema, lesions may Figure 23–1 Eczematous dermatitis. A, The patterned erythema and
be widely distributed. Spongiosis, or epidermal edema, scale stems from a nickel-induced contact dermatitis produced by this
characterizes all forms of acute eczematous dermatitis— woman’s necklace. B, Microscopically, there is fluid accumulation (spon-
hence the synonym spongiotic dermatitis. Edema fluid giosis) between epidermal cells that can progress to small vesicles if
seeps into the epidermis, where it splays apart keratinocytes intercellular connections are stretched until broken.
(Fig. 23–1, B). Intercellular bridges are stretched and become penicillin, salicylates, hydantoins, and antimalarials.
more prominent and are easier to visualize. This change is Patients present with a wide diversity of lesions (hence called
accompanied by a superficial perivascular lymphocytic infil- “multiforme”) including macules, papules, vesicles, and bullae,
trate, edema of dermal papillae, and mast cell degranulation. as well as characteristic targetoid lesions consisting of red
Eosinophils may be present and are especially prominent in macules or papules with pale vesicular or eroded centers (Fig.
spongiotic eruptions provoked by drugs, but in general the 23–2). The epithelial damage is believed to result from the
histologic features are similar regardless of cause, emphasiz- action of skin-homing cytotoxic T cells that attack the basal
ing the need for careful clinical correlation. cells of the skin and the mucosae, which may display anti-
gens that cross-react with the inciting drug or microbe.
Clinical Features
Lesions of acute eczematous dermatitis are pruritic (itchy), MORPHOLOGY
edematous, oozing plaques, often containing vesicles and
bullae. With persistent antigen exposure, lesions may Well-developed lesions have a characteristic “targetoid”
become progressively scaly (hyperkeratotic) as the epider- appearance (Fig. 23–2, A). Early lesions show a superficial
mis thickens (acanthosis). Some changes are produced or perivascular, lymphocytic infiltrate associated with dermal
exacerbated by scratching or rubbing of the lesion (see later edema and margination of lymphocytes along the dermoepi-
under “Lichen Simplex Chronicus”). The clinical causes of dermal junction in intimate association with degenerating
eczema are sometimes divided into “inside jobs”—reaction
to an internal circulating antigen (such as ingested food or
drug)—and “outside jobs”—disease resulting from contact
with an external antigen (such as poison ivy).

Susceptibility to atopic dermatitis is often inherited; the
disorder is concordant in 80% of identical twins and 20%
of fraternal twins. It usually appears in early childhood and
in the majority of cases clears in adults. Children with
atopic dermatitis often have asthma and allergic rhinitis,
termed the atopic triad.

Erythema Multiforme

Erythema multiforme is an uncommon, usually self-limited
disorder that appears to be a hypersensitivity response to
certain infections and drugs. Antecedent infections include
herpes simplex and those caused by mycoplasmas and
some fungi. The implicated drugs include sulfonamides,