Case Based Pediatrics For Medical Students and Residents
Department of Pediatrics, University of Hawaii John A. Burns School of Medicine
Chapter XXI.1. Eczematous Dermatitis (Atopic Dermatitis and Seborrhea)
M. Stanton Michels, MD
January 2002

Return to Table of Contents

This is a 2 year old toddler who has had "bad skin" since soon after he was born. He had "cradle cap" as an infant that became generalized to his face, and from there to his upper torso. Off and on throughout his life, he has had "flare-ups" of erythematous, scaling patches on his cheeks, chest and abdomen. His mother expresses frustration with the doctors' inability to help her son's skin. She has used moisturizers and 1% hydrocortisone cream episodically in the past. Presently his hands are so inflamed, cracked and bleeding that he doesn't move his fingers much. "He never stops scratching!", she declares. She admits however that they are more successful in controlling his asthma that was diagnosed about one year ago.


Atopic dermatitis (AD) largely starts in infancy and early childhood. 85% of cases first present before the fifth birthday. Common manifestations can include pruritus (which is universal), lichenification and linear cracking in those flexural areas, xerosis (dry flakey skin generally prior to the patchy outbreaks), periauricular fissures, cheilitis (inflammation and cracking of lips, particularly at the corners of the mouth), scalp dermatitis (e.g., cradle cap), and susceptibility to cutaneous infections by S. aureus.

Epidemiologically, atopic dermatitis seems to be increasing worldwide. Exact figures are lacking; however since there is not a strict method of defining the disease. There does seem to be some variation in rates from one ethnic or geographic area to another. Reported rates can run from greater than 20% in Scandinavian populations to less than 5% in east Africa.

Some would offer the diagnostic criteria of: itchy skin (mandatory for the diagnosis) plus at least 3 of the following:
. . . . . 1) Involvement of the skin creases.
. . . . . 2) Past medical history of asthma or hay fever.
. . . . . 3) History of generally dry skin.
. . . . . 4) Onset less than age 2 years.
. . . . . 5) Visible flexural dermatitis.

Other objective tests useful in the diagnosis might include total IgG and increased IgE. Genetics seems to play an important factor. Co-twin studies have shown a high concordance for the disease in identical twins over dizygotic twins. In addition, there is a strong relationship between atopic dermatitis and other allergic disease manifestations such as asthma and allergic rhinitis. AD characteristically displays two immune responses: 1) IgE overproduction, and 2) diminished cell mediated immunity. Cytokines, particularly IL-4 produced by T cells, seem to promote IgE production. It is hypothesized that an overwhelming T-cell activity which produces this aberrant lymphokine profile limits cellular immune response. This in turn may increase susceptibility to certain microorganisms. Interestingly, house dust mite, cat dander, and certain pollens have been related to atopic dermatitis exacerbations.

The question of food allergy is often posed by parents, but the connection to food allergies is less clear. The consensus is that food can play a role in certain individuals. Finding the specific food precipitant, however, is usually a time consuming and frustrating process. Although the literature is somewhat conflicting, it is generally held that less than 10% of AD children can be shown to have a specific food as a cause for their dermatitis. Skin testing or RAST blood tests are often not helpful in the diagnosis. Having said this, the most common offending agents, when one is identified, are eggs, milk, seafood, nuts, wheat, and soy. Elimination diets may not in the end alter the natural course of atopic dermatitis. Eczematous reactions may not become apparent until several days after the ingestion.

Differential diagnosis largely depends on the age and distribution of the rash. Although there is some dispute on the nomenclature, many authors would lump atopic dermatitis and seborrhea together in a group of eczematoid dermatitis. They stress that atopic dermatitis often occurs in individuals who had seborrheic dermatitis in infancy. There are some differences however. In early infancy, seborrheic dermatitis usually presents earlier than 2 months of age with AD presenting thereafter. Seborrhea has a much better prognosis, and usually resolves by six months of age, just when atopic dermatitis becomes more prevalent. Pruritus is not customarily a big factor in seborrhea, but is always present in AD. There are patches of erythema which usually start on the scalp and move down over the face and cheeks. These red patches scale and have an oily appearance. The rash itself is difficult to distinguish morphologically from atopic dermatitis. In older children, scabies can cause discrete areas of pruritus with papular erythema, but usually these show a predilection for the hands, feet, and genital areas. One will often find the tiny burrow wounds on close inspection (often in the web spaces between the fingers). Allergic contact dermatitis is more sudden in onset and less relapsing in course. Usually a specific new allergen can be identified by history. Very specific distribution is often helpful.

There are several more severe immune disorders that may be entertained. Hyper IgE syndrome (Job's syndrome) often produces more severe infections of tissues other than the skin, such as pneumonias, sinusitis, or deep soft tissue abscesses. Wiskott-Aldrich syndrome can produce flexural dermatitis which appears clinically as AD, and X-linked Bruton's agammaglobulinemia can also produce similar rashes, but shows low IgE levels. Histiocytosis-X can also present with patchy erythematous, pruritic rash.

As is the case with acne, the level of therapy should be tailored to the severity of the disease. Generally, AD patients are found to have dry skin, which may produce cracking that contributes to antigen stimulation of the deeper tissues. Without a doubt, moisturizers hold a key role in providing a barrier to this drying. Emollients are best, but a very greasy product may not be well tolerated by older patients although they form the best barrier. Systemic antihistamines may help with pruritus, and the more sedating of these, such as hydroxyzine, seem to have the greatest effect, particularly in younger children to avoid bed time scratching.

Corticosteroids form the main line of therapy. These should be started with 1% hydrocortisone, which is the mildest of the group. For more resistant cases, one will probably have to use fluorinated, high potency steroid preparations. Triamcinolone cream 0.1% can be used for flare ups. Very occasionally, particularly severe, body wide exacerbations, may require short bursts of systemic steroids (1-3 mg/kg per day of oral prednisolone), which is often successful in improving the severe exacerbation within a few days. There is a concern of systemic absorption of topical steroids, but many studies have failed to show an actual adverse effect unless there was long term use. However, potent topical corticosteroids, if used repeatedly or over long term, can cause skin thinning and striae. Should these measures fail, some have used tar or ichthammol. PUVA (psoralen + ultraviolet A light) enhances the absorption of UV-A selectively into the affected skin lesions. Cyclosporin has also been used.

Newer medications called non-steroid immunomodulators, tacrolimus (Protopic) and pimecrolimus (Elidel), are approved by the FDA (since 2000) for atopic dermatitis. Unlike corticosteroids, these can be safely used for long periods of time without the corticosteroid side effects of skin thinning and telangiectasia.

Seborrheic dermatitis is usually managed somewhat differently than AD. There is an overproduction of oil on the scalp which combines with superficial exfoliated cells of epidermis to form the scales that are so prevalent. Oils therefore tend to worsen this condition so that moisturizers are actually contraindicated. Indeed, when parents, thinking that the scales indicate dry skin, rub oil into the scalp of their baby, the condition usually worsens. Parents should be instructed to shampoo the scalp with mild baby shampoo and gently try to remove the flakes and scales with their fingers. When the condition creeps down onto the face, however, mild corticosteroid creams can provide great relief as is the case with atopic dermatitis.


Questions

1. True/False: Seborrhea starts in infancy at the same time as atopic dermatitis.

2. True/False: Many infants who have seborrhea will eventually develop atopic dermatitis.

3. True/False: The prevalence of atopic dermatitis is generally higher in more developed societies and may be in part related to diverse environmental stimuli present in these communities.

4. Which of the following is a true statement?
. . . . . a. Seborrhea produces dry scales on the scalp of infants.
. . . . . b. Both seborrhea and atopic dermatitis benefit from scale removal.
. . . . . c. Seborrhea is not pruritic.
. . . . . d. Hydrocortisone cream can be used in cradle cap dermatitis.

5. A 5 year old child presents with a red, itchy rash in a 2 cm band across his abdomen below the umbilicus. The most likely diagnosis is:
. . . . . a. Contact dermatitis
. . . . . b. Scabies
. . . . . c. Atopic dermatitis
. . . . . d. Shingles


References

1. Hanifin JM. Atopic Dermatitis in Infants and Children. Pediatr Clin North Am 1991;38(4)763-789.

2. Hywel WC. Pediatric Dermatology, 2nd edition. 1996, New York: Churchill Livingstone, pp. 161-258 .

3. Krafchic BR. Textbook of Pediatric Dermatology. 2000, Blackwell Science, LTD. pp. 685-707.


Answers to questions

1.False, 2.True, 3.True, 4.c, 5.a


Return to Table of Contents

University of Hawaii Department of Pediatrics Home Page