Page 94 - The Netter Collection of Medical Illustrations - Integumentary System_ Volume 4 ( PDFDrive )
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Plate 4-9 Integumentary System
ADOLESCENTS AND ADULTS WITH ATOPIC DERMATITIS
Scalp, facial, and truncal
atopic dermatitis in a child
ATOPIC DERMATITIS
(Continued)
Pathogenesis: The cause of atopic dermatitis is
unknown. Many exacerbating factors have been found.
They include anything that irritates the skin, such as
heat, sweating, stress, many chemicals, and various
types of clothing. Atopic dermatitis is believed to be
caused by an aberrant T-cell (Th2) response in the skin
with elevated levels of Th2 cytokines. Interleukin-4
(IL-4), IL-5, and IL-13 are abnormally elevated. These
cytokines are responsible for eosinophil production and
recruitment and for IgE production. The concentra-
tions of the Th1 cytokines (IL-12 and interferon-α) are
below average in these patients. The reason for this
response is unknown. Ultimately, the barrier of the
epidermis is disrupted, and this is evident by the
increase in transepidermal water loss, which can be
measured.
Histology: A nonspecific lymphocytic infiltrate is
seen, with associated exocytosis of lymphocytes into the
epidermis with widespread spongiosis. Varying degrees
of acanthosis and parakeratosis are seen. Often, bacte-
rial elements are seen on the surface of the skin. Small
intraepidermal vesicles may develop secondary to the
massive spongiosis. Excoriations are frequently seen.
Treatment: Therapy consists of patient and family
education about the natural history of the disease and
the episodic waxing and waning. Bathing regimens
must be thoroughly explained, and the use of soap Adult patient with atopic
should be discouraged. The patient should take shorter dermatitis
baths in lukewarm water, followed immediately
by moisturization and application of topical steroid Adult atopic dermatitis
medications as appropriate. The intermittent use of can also be complicated by
moisturizers is also helpful. The use of topical immu- allergic contact dermatitis.
nomodulators, alternating with topical corticosteroids
or alone, decreases the atrophogenic side effects of the
topical corticosteroids. On occasion, oral steroids may
be needed to calm the inflammation and give the patient
some well-needed, albeit temporary, relief.
Most children do not need to avoid foods. If any
question exists as to whether a food is potentially exac-
erbating the dermatitis, an allergist may be consulted
to perform specific food allergy testing.
Prompt recognition of any bacterial or viral infec-
tion should lead to therapy that is not delayed. Impe- differentiate herpes simplex virus from varicella zoster subset of patients respond to ultraviolet phototherapy,
tigo, molluscum contagiosum, and eczema herpeticum virus. A viral culture or direct immunofluorescence but most are not able to tolerate the warmth and sweat-
are the three infections most commonly associated antibody staining of blister fluid is required for ing that is induced by the phototherapy unit. Oral
with atopic dermatitis. Of these, eczema herpeticum is differentiation. immunosuppressants are used and include cyclosporine,
the most important, and its recognition depends on Treatment is usually more successful in children than azathioprine, and mycophenolate mofetil. These medi-
a strong index of suspicion in any child with atopic in adults. Occasionally in children and more commonly cations have severe potential side effects and should be
dermatitis and new onset of a widespread, blistering in adults, systemic therapies are used to keep the der- administered only by experienced clinicians. Routine
rash. The differential diagnosis is varicella. A Tzanck matitis under control. Oral antihistamines and immu- laboratory testing is required with all of these
test can help diagnosis the condition but cannot nosuppressive agents are not uncommonly required. A medications.
80 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

