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.