ATOPIC DERMATITIS
Atopic
dermatitis is one of the most common dermatoses of childhood. It typically
manifests in early life and can have varying degrees of expression. It is
commonly associated with asthma and allergies. Most children eventually outgrow
the condition. Atopic dermatitis has been estimated to affect up to 10% of all
children and 1% of adults, and its prevalence has been steadily increasing.
Patients frequently have a family history of atopic dermatitis, asthma, or skin
sensitivity.
 |
| INFANTS AND CHILDREN WITH ATOPIC DERMATITIS |
Clinical Findings: Atopic
dermatitis typically begins early in life. There is no racial predilection. The
clinical course is often chronic, with a waxing and waning nature. Infants a
few months old may initially present with pruritic, red, eczematous patches on
the cheeks and extremities as well as the trunk. The itching is typically
severe and causes the child to excoriate the skin, which can lead to secondary
skin infections. The skin of atopics is abnormally dry and is sensitive to heat
and sweating. These children have difficulty sleeping because of the severe
pruritus associated with the rash. During flares of the dermatitis, patients
may develop weeping patches and plaques that are extremely pruritic and
occasionally painful. With time, the patches begin to localize to flexural
regions, particularly the antecubital and popliteal fossae. Severely afflicted
children may have widespread disease. Patients with atopic dermatitis are more
prone to react to contact and systemic allergens. Sensitivity to contact
allergens is likely a consequence of the frequent use of topical medicaments
and the broken skin barrier. This combination leads to increased exposure to
foreign antigens that are capable of inducing allergic contact dermatitis. One
should suspect a coexisting contact dermatitis if a patient who is doing well
experiences a flare for no apparent reason or if a patient continues to get
worse despite aggressive topical or oral therapy. Laboratory testing commonly
shows an eosinophilia and an elevated immunoglobulin E (IgE) level.
Secondary infection is common in
atopic dermatitis. It may manifest with the appearance of honey-colored,
crusted patches in the excoriated regions, which indicates impetigo. It may
also manifest as multiple follicle-based pustules, representing folliculitis,
or as deep red, tender macules, indicating a deeper soft tissue infection. The
rate of methicillin-resistant Staphylococcus aureus (MRSA) infection has
increased in patients with atopic dermatitis at the same rate as in the general
public. The rate of colonization of atopic patients is much higher than in
normal controls, most likely because of the disruption of the underlying
epidermis. Colonization in certain situations may lead to infection.
Acquisition of a widespread herpesvirus infection can have severe and
potentially life-threatening consequences. Atopics are much more prone than
others to develop eczema herpeticum. The extensive areas of abnormal, broken
skin provide the perfect environment for the development of this wide- spread
viral infection.
Most childhood atopic dermatitis
resolves spontaneously over time. It is estimated that 10% of cases will
resolve by the age of 1 year, 50% by 5 years, 70% by 7 years, and so on. A
small percentage of children with atopic dermatitis continue on with the rash
into adult-hood. These cases tend to be chronic in nature and to last for the
patient’s lifetime.
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 concentrations 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, bacterial elements are seen on
the surface of the skin. Small intraepidermal vesicles may develop secondary to
the massive spongiosis. Excoriations are frequently seen.
 |
| ADOLESCENTS AND ADULTS WITH ATOPIC DERMATITIS |
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 should be discouraged. The patient should take
shorter baths in lukewarm water, followed immediately by moisturization and
application of topical steroid medications as appropriate. The intermittent use
of moisturizers is also helpful. The use of topical immunomodulators,
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
exacerbating the dermatitis, an allergist may be consulted to perform specific
food allergy testing.
Prompt recognition of any
bacterial or viral infection should lead to therapy that is not delayed.
Impetigo, molluscum contagiosum, and eczema herpeticum are the three infections
most commonly associated with atopic dermatitis. Of these, eczema herpeticum is
the most important, and its recognition depends on a strong index of suspicion in
any child with atopic dermatitis and new onset of a widespread, blistering
rash. The differential diagnosis is varicella. A Tzanck test can help diagnosis
the condition but cannot differentiate herpes simplex virus from varicella
zoster virus. A viral culture or direct immunofluorescence antibody staining of
blister fluid is required for differentiation.
Treatment is usually more
successful in children than in adults. Occasionally in children and more
commonly in adults, systemic therapies are used to keep the dermatitis under
control. Oral antihistamines and immunosuppressive agents are not uncommonly
required. A subset of patients respond to ultraviolet phototherapy, but most
are not able to tolerate the warmth and sweating that is induced by the phototherapy
unit. Oral immunosuppressants are used and include cyclosporine, azathioprine,
and mycophenolate mofetil. These medications have severe potential side effects
and should be administered only by experienced clinicians. Routine laboratory t
sting is required with all of these medications.
