CASE #2: Atopic dermatitis

Facial rashes on children can be distressing for the patient and a challenge for the clinician. Atopic dermatitis (AD), or eczema, is a common chronic skin disorder that often begins early in childhood.2 This disorder can affect any area of the body, but the face is most commonly involved, especially in children. Extreme temperatures are known flares, and dry winters are especially bad. Children with AD can experience periods of remission lasting months or even years. The incidence among adults is approximately 0.9%, with many of these individuals developing AD only in adulthood, when it tends to localize to flexural folds.

Examination showed an extensive scaly rash with well-defined annular borders covering the central part of the face, including the cheeks and eyelids. A KOH preparation failed to show any fungal elements. The child’s skin was extraordinarily dry and flaky. She had been diagnosed with mild asthma at age 2 years and had demonstrated numerous signs of seasonal allergies (i.e., congestion, rhinitis, and conjunctivitis). A sibling and the child’s father shared a similar history.


Continue Reading

AD is characterized by pruritus, xerosis, eczematous rashes, and eventual lichenification. There is often a personal and family history of such atopic conditions as seasonal allergies and asthma. Minor diagnostic criteria include hyperlinear palms, keratosis pilaris, chelitis, nipple eczema, and sweat-induced pruritus.

Emotional factors play a major role in exacerbations of AD. The disease can contribute to a wide variety of stressors, including loss of sleep and pruritus, that keep the patient in an itch-scratch-itch cycle that is difficult to control (especially in children).3

The prevalence of AD in this country is estimated to be as high as 30%,2 but the rate is climbing worldwide, especially in developed countries. In contrast, the rate in China and Iran is estimated at 2%-3%. Blacks and Asians are more prone to AD than whites.2

Among children with AD, 85% of will develop it in their first year of life. Eczema manifests with scaly, red rashes on the face, scalp, and trunk. Diaper rash is especially common in these infants, a phenomenon that speaks to the basic causes of AD.

In healthy people, there is a natural balance between the TH1 and TH2 subdivisions of T-cells. In people with AD, it is theorized that TH2 cells predominate, leading to the production of increased levels of cytokines. This in turn produces interleukins, leading to increased levels of immunoglobulin E.

A competing theory holds that defects in barrier function in the outermost layer of skin (the stratum corneum) allows antigens to penetrate into the dermis, leading to increased levels of pro-inflammatory cytokines. These same antigens can be absorbed from the gut and lungs, but whether these play a role in the development of AD is highly debatable. Studies regarding the role of certain foods (e.g., milk and eggs) have produced conflicting results.

In AD, transepidermal water loss is increased, and defective lamellar bodies may be caused by abnormalities of ceramide production, leading to or worsening diminished barrier function. Inherited defects in filaggrin structure and function affect a significant percentage of AD patients, causing epithelial disruption that allows penetration of allergens. Which of these factors are primary or secondary is yet to be understood.

While individuals with AD are highly susceptible to skin infections of all kinds, they are particularly prone to staphylococcal infections. Large numbers of this organism colonize the lesional skin of AD sufferers and may be a major factor in flares. In such cases, oral antibiotics can be extremely helpful.

People with AD are also extraordinarily susceptible to viral infections of the skin, especially herpes simplex virus (HSV), human papillomavirus, and the poxvirus that causes molluscum contagiosum. While the latter two are more of a nuisance, HSV can produce severe disease in these patients, including a disseminated version called eczema herpeticum, which can be recurrent.

The differential diagnosis for AD is broad and includes contact vs. irritant dermatitis, seborrheic dermatitis, simple xerosis, psoriasis, and dermatophytosis, to name a few. The diagnosis of AD is greatly simplified by knowing how utterly common it is and searching for corroborative physical and historical findings.

Successful treatment requires extensive patient education tailored to eliminate misunderstanding and the counterproductive measures that are often used initially. For example, pointing out the inherited basis for AD is a useful point of departure. Similarly, emphasize the likely benign prognosis, stressing the issues of xerosis and barrier-function issues and the need for regular use of appropriate moisturizers and avoidance of scented/perfumed products.

For the pruritus, the use of topical steroids is appropriate as long as proper strengths and vehicles are used and accompanied by age-appropriate advice about frequency and duration of application.

In cases in which secondary bacterial infection or colonization is suspected, seven- to 10-day courses of oral antibiotics (e.g., sulfamethoxazole/trimethoprim [Bactrim, Cotrim, Septra] or cephalexin [Keflex]) can be quite useful. Oral antihistamines are useful as sedatives but do little for the basic pathologic process. Oral glucocorticoids (e.g., prednisone or methylprednisolone [Medrol]) are frequently used for refractive cases of AD, but their use is potentially problematic and subject to restrictions that are beyond the scope of this article. n

Mr. Monroe is a physician assistant specializing in dermatology at Springer Clinic in Tulsa, Okla. He has no relationships to disclose relating to the contents of this article.



References

1. eMedicine. Tinea facei.

2. eMedicine. Atopic dermatitis.

3. Odom RB, James WD, Berger TG, eds. Andrews’ Diseases of the Skin: Clinical Dermatology. 10th ed. Philadelphia, Pa.: Saunders; 2006:66-69.

All electronic documents accessed January 15, 2011.